Echinacoside has various pharmacological effects, such as antioxidative, antisenescence, neuroprotection, antiinflammation, promotion of cicatrization, hepatoprotection, promotion of bone formation, and antitumor activity. There are some progress in its pharmacokinetics study. Echinacea has therapeutic effect on diseases in various systems. It has great significance to further research and develop echinacoside.
骨质疏松症是发病率较高的骨疾病,尤其是绝经后妇女。松果菊苷具有雌激素样作用,对骨质疏松,尤其是雌激素降低引起的骨质疏松具有良好疗效。LI等[28]通过切除卵巢建立大鼠骨质疏松模型,用松果菊苷处理后,大鼠尿中钙磷显著下降,骨矿物密度(bone mineral density, BMD)升高,大鼠骨质增多,并且增加了骨形成和降低了骨吸收,对大鼠雌激素缺乏引起的骨质疏松有较好的治疗作用。松果菊苷还能够促进细胞增殖、提高碱性磷酸酶(alkaline phosphatase,ALP)水平、升高胶原蛋白-1(collagen I, COL I)和骨钙蛋白(osteocalcin, OCN)浓度,能有效刺激骨形成,对抗骨质疏松[29]。另外,YANG等[30]也提出,松果菊苷可以改善模型鼠股骨的BMD和骨微结构,增加骨保护素(osteoprotegerin, OPG)的水平,降低核因子受体激活因子配体(receptor activator of nuclear factor-κB ligand, RANKL)水平,对雌激素缺乏引起的骨质疏松有良好疗效。雌激素治疗盆底功能障碍性疾病一直存在争议,主要在于雌激素副作用较多,但是植物雌激素副作用少且轻,松果菊苷应用于妇科疾病值得期待。
CARSTENSENS, BONARJEE VV, BERNINGJ, et al.Effects of early enalapril treatment on global and regional wall motion in acute myocardial infaraion[J]. Am Heart J, 1995, 129(6): 1101-1108.
CERVELLATIR, RENZULLIC, GUERRA MC, et al.Evaluation of antioxidant activity of some natural polyphenolic compounds using the Briggs-Rauscher reaction method[J]. J Agric Food Chem, 2002, 50(26): 7504-7509.
A new method based on the inhibitory effects of antioxidants on the oscillations of the hydrogen peroxide, acidic iodate, malonic acid, and Mn(II)-catalyzed system (known as the Briggs-Rauscher reaction), was used for the evaluation of antioxidative capacity. With this method, which works near the pH of the fluids in the stomach (pH approximately 2), a group of natural compounds present in fruits and vegetables or in medicinal plants assumed to have antioxidant capacity, was tested successfully. The aim of the present study is to evaluate the antioxidative properties of some active principles contained in vegetables and aromatic plants, namely, cynarin (from Cynara scolymus), rosmarinic acid (from Rosmarinus officinalis), echinacoside (from Echinacea species), puerarin (from Pueraria lobata), and oleuropein (from Olea europea). Also studied with the Briggs-Rauscher reaction method was the antioxidant activity of cyanidin 3-O-beta-glucopyranoside (from Citrus aurantium) in order to compare the results with those obtained by other methods. The conclusions on the dependency of the antioxidative activity on the pH of the testing system are given.
WUY, LIL, WENT, et al.Protective effects of echinacoside on carbon tetrachloride-induced hepatotoxicity in rats[J]. Toxicology, 2007, 232(1/2): 50-56.
The aim of this study was to investigate the possible protective effects of echinacoside, one of the phenylethanoids isolated from the stems of Cistanches salsa, a Chinese herbal medicine, on the free radical damage of liver caused by carbon tetrachloride in rats. Treatment of rats with carbon tetrachloride produced severe liver injury, as demonstrated by dramatic elevation of serum ALT, AST levels and typical histopathological changes including hepatocyte necrosis or apoptosis, haemorrhage, fatty degeneration, etc. In addition, carbon tetrachloride administration caused oxidative stress in rats, as evidenced by increased reactive oxygen species (ROS) production and MDA concentrations in the liver of rats, along with a remarkable reduction in hepatic SOD activity and GSH content. However, simultaneous treatment with echinacoside (50mg/kg, intraperitoneally) significantly attenuated carbon tetrachloride-induced hepatotoxicity. The results showed that serum ALT, AST levels and hepatic MDA content as well as ROS production were reduced dramatically, and hepatic SOD activity and GSH content were restored remarkably by echinacoside administration, as compared to the carbon tetrachloride-treated rats. Moreover, the histopathological damage of liver and the number of apoptotic hepatocytes were also significantly ameliorated by echinacoside treatment. It is therefore suggested that echinacoside can provide a definite protective effect against acute hepatic injury caused by CCl(4) in rats, which may mainly be associated with its antioxidative effect.
DENGM, ZHAO JY, TU PF, et al.Echinacoside rescues the SHSY5Y neuronal cells from TNF-ainduced apoptosis[J]. Eur J Pharmacol, 2004, 505(1): 11-18.
Aim To investigate the neuroprotective e ffect of echinacoside, one of the phenylethanoids isolated from Cistanche salsa, on tumor necrosis factor-alpha (TNFα)-induced apoptosis in SH-SY5Y neuronal cells. Methods Cell viability was analyzed using MTT assay. Apoptotic cells were detected using DNA fragmentation and flow cytometric analys is. The level of intracellular reactive oxygen species(ROS) and the potential of mitochondrial membrane were determined by laser scanning confocal microscopy (L SCM). The activity of caspase-3 was measured with microplate spectrofluorometer . Results Treatment of cultured SH-SY5Y cells with 100 μg· L -1 TNFα for 36 h induced a significant decrease of cell viability, and t he percentage of apoptosis increased to 37%. The level of intracellular ROS and activity of caspase-3 enhanced, and the red/green ratios of mitochondrial membr ane decreased to 0.35 from 5.97. However, simultaneous treatment with echinac oside (1, 10, or 100 mg·L -1) exhibited cytoprotective effects, reduced fo rmation of the DNA ladder, prevented the accumulation of ROS and caspase-3, reconverted the potential of mitochondrial membrane, and the percentage of apoptosis/necrosis neurons was significantly decreased to 25.9%, 18.3% and 8.2% in a dose-dependent manner . Conclusion These results demonstrate that echinacoside has the neuroprotective capacity to antagonize TNFα-induced apoptosi s in SH-SY5Y cells. The antiapoptotic action of echinacoside may be partially d ependent on an anti-oxidative stress effects, inhibition of caspase-3 activity , and maintain of mitochondria function.
DIZDAROGLUM, JARUGAP, BIRINCIOGLUM, et al.Free radical-induced damage to DNA: mechanisms and measurement[J]. Free Radic Biol Med, 2002, 32(11):1102-1115.
Free radicals are produced in cells by cellular metabolism and by exogenous agents. These species react with biomolecules in cells, including DNA. The resulting damage to DNA, which is also called oxidative damage to DNA, is implicated in mutagenesis, carcinogenesis, and aging. Mechanisms of damage involve abstractions and addition reactions by free radicals leading to carbon-centered sugar radicals and OH- or H-adduct radicals of heterocyclic bases. Further reactions of these radicals yield numerous products. Various analytical techniques exist for the measurement of oxidative damage to DNA. Techniques that employ gas chromatography (GC) or liquid chromatography (LC) with mass spectrometry (MS) simultaneously measure numerous products, and provide positive identification and accurate quantification. The measurement of multiple products avoids misleading conclusions that might be drawn from the measurement of a single product, because product levels vary depending on reaction conditions and the redox status of cells. In the past, GC/MS was used for the measurement of modified sugar and bases, and DNA-protein cross-links. Recently, methodologies using LC/tandem MS (LC/MS/MS) and LC/MS techniques were introduced for the measurement of modified nucleosides. Artifacts might occur with the use of any of the measurement techniques. The use of proper experimental conditions might avoid artifactual formation of products in DNA. This article reviews mechanistic aspects of oxidative damage to DNA and recent developments in the measurement of this type of damage using chromatographic and mass spectrometric techniques.
KUANGR, SUNY, YUANW, et al.Protective effects of echinacoside, one of the phenylethanoid glycosides, on H2O2-induced cytotoxicity in PC12 cells[J]. Planta Med, 2009, 75(14): 1499-1504.
We have investigated the protective effects of echinacoside (ECH), one of the phenylethanoid glycosides, on H
REHMAN SU, SHAH SA, ALIT, et al.Anthocyanins reversed D-galactose-induced oxidative stress and neuroinflammation mediated cognitive impairment in adult rats[J]. Mol Neurobiol, 2016(1):1-17.
Aging is a major factor involved in neurological impairments, decreased anti-oxidant activities, and enhanced neuroinflammation. D-galactose (D-gal) has been considered an artificial aging model which
CHENS, FENGH, SHERCHANP, et al.Controversies and evolving new mechanisms in subarachnoid hemorrhage[J]. Prog Neurobiol, 2014,115(1): 64-91.
Despite decades of study, subarachnoid hemorrhage (SAH) continues to be a serious and significant health problem in the United States and worldwide. The mechanisms contributing to brain injury after SAH remain unclear. Traditionally, most in vivo research has heavily emphasized the basic mechanisms of SAH over the pathophysiological or morphological changes of delayed cerebral vasospasm after SAH. Unfortunately, the results of clinical trials based on this premise have mostly been disappointing, implicating some other pathophysiological factors, independent of vasospasm, as contributors to poor clinical outcomes. Delayed cerebral vasospasm is no longer the only culprit. In this review, we summarize recent data from both experimental and clinical studies of SAH and discuss the vast array of physiological dysfunctions following SAH that ultimately lead to cell death. Based on the progress in neurobiological understanding of SAH, the terms “early brain injury” and “delayed brain injury” are used according to the temporal progression of SAH-induced brain injury. Additionally, a new concept of the vasculo-neuronal-glia triad model for SAH study is highlighted and presents the challenges and opportunities of this model for future SAH applications.
TANS, WOODM, MAHERP.Oxidative stress induces a form of programmed cell death with characteristics of both apoptosis and necrosis in neuronal cells[J]. J Neurochem, 1998, 71(1): 95-105.
Abstract Oxidative stress is implicated in a number of neurological disorders including stroke, Parkinson's disease, and Alzheimer's disease. To study the effects of oxidative stress on neuronal cells, we have used an immortalized mouse hippocampal cell line (HT-22) that is particularly sensitive to glutamate. In these cells, glutamate competes for cystine uptake, leading to a reduction in glutathione and, ultimately, cell death. As it has been reported that protein kinase C activation inhibits glutamate toxicity in these cells and is also associated with the inhibition of apoptosis in other cell types, we asked if glutamate toxicity was via apoptosis. Morphologically, glutamate-treated cells underwent plasma membrane blebbing and cell shrinkage, but no DNA fragmentation was observed. At the ultrastructural level, there was damage to mitochondria and other organelles although the nuclei remained intact. Protein and RNA synthesis inhibitors as well as certain protease inhibitors protected the cells from glutamate toxicity. Both the macromolecular synthesis inhibitors and the protease inhibitors had to be added relatively soon after the addition of glutamate, suggesting that protein synthesis and protease activation are early and distinct steps in the cell death pathway. Thus, the oxidative stress brought about by treatment with glutamate initiates a series of events that lead to a form of cell death distinct from either necrosis or apoptosis.
ZHUM, LUC,LIW.Transient exposure to echinacoside is sufficient to activate Trk signaling and protect neuronal cells from rotenone[J]. J Neurochem, 2013, 124(4): 571-580.
ABSTRACT Neurotrophins exert their physiological functions mainly through Trk receptors, and the neurotrophic signaling network is critical to the survival of neurons. However, therapeutic use of neurotrophins in treating neurodegenerative diseases is hampered by a number of pharmacological challenges, and the most significant challenge is their delivery into the central nervous system. Here we reported that echinacoside, a small natural compound, elicits neuroprotection by activating Trk receptors and their downstream signal pathways. Echinacoside is the major active component of Cistanches Herba, a widely used Chinese herb with neuroprotective effects. We showed in this present study that transient exposure to echinacoside is sufficient to protect neuronal cells and non-neuronal cells overexpressed with TrkA or TrkB against rotenone injury. Additional investigations on the mechanisms underlying suggested that transient treatment with echinacoside inhibits cytochrome c release and caspase-3 activation caused by ensuing rotenone exposure via activating Trk-ERK pathway in neuronal cells. Since echinacoside is able to cross the blood-brain barrier freely, it may have a promising potential in neurodegenerative diseases treatment. 漏 2012 International Society for Neurochemistry, J. Neurochem. (2012) 10.1111/jnc.12103.
FENG XY, ZHUM, ZHANG QQ, et al.Selective protection of nigral dopaminergic neurons by echinacoside in a rat model of Parkinson’s disease induced by rotenone[J].J Chin Integra Med, 2012,10(7): 777-783.
Abstract OBJECTIVE: To observe the protective effects of echinacoside on rotenone-induced damages in rats. METHODS: Healthy male Sprague-Dawley rats, weighing from 200 to 220 g, were randomly divided into five groups with 20 rats in each group: control group, rotenone group and echinacoside groups of low, medium and high doses (20, 40 and 80 mg/(kg路d)). Rats in the rotenone group were injected intraperitoneally for four weeks with rotenone (2.75 mg/(kg路d)), dissolved into dimethyl sulfoxide; rats in the control group were injected intraperitoneally with dimethyl sulfoxide daily, and rats in the echinacoside groups received daily intraperitoneal injection of rotenone along with echinacoside gastric perfusion for four weeks. Modified neurological severity score was used to evaluate neurobehavior of the animals; dopaminergic neurons in substantia nigra were observed by immunochemical method and dopamine concentration in striatum was determined by a fluorescence spectrophotometer. Biomarkers of liver and kidney damage were also measured. RESULTS: In the rotenone group, the rats suffered from severe neurological disability (P0.05). CONCLUSION: Rotenone causes severe damages to dopaminergic neurons, liver and kidney in rats and echinacoside selectively reverses dopaminergic neuronal injury.
WEI LL, CHENH, JIANGY, et al.Effects of echinacoside on histio-central levels of active mass in middle cerebral artery occlusion rats[J]. Biomed Environ Sci, 2012, 25(2): 238-244.
These results imply that echinacoside may protect striatal dopa minergic neurons from the injury induced by MCAO and may help prevent and treat cerebral ischemic diseases.
CHENH, JING FC, LI CL, et al.Echinacoside prevents the striatal extracellular levels of monoamine neurotransmitters from diminution in 6-hydroxydopamine lesion rats[J]. J Ethnopharmacol, 2007, 114(3): 285-289.
We investigated the effects of echinacoside, a phenylethanoid glycoside isolated and purified from the stems of Cistanche salsa, a Chinese herbal medicine, on the striatal extracellular levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in 6-hydroxydopamine (6-OHDA) lesion rats. Seven days after 6-OHDA was injected into the right striatum of rats, the striatal extracellular levels of DA, DOPAC and HVA fell significantly (P<0.01 vs. vehicle), as demonstrated by the method of cerebral microdialysis and high performance liquid chromatography with electrochemical detection. However, simultaneous treatment with echinacoside (7.0, 3.5mg/kg) attenuated the diminution of them (P<0.01 vs. model). The results implied that echinacoside could protect the striatal dopaminergic neurons from injury induced by 6-OHDA and may be useful in the prevention and treatment of Parkinson's disease (PD).
WANG YH, XUAN ZH, TIANS, et al.Echinacoside protects against 6-hydroxydopamine-induced mitochondrial dysfunction and inflammatory responses in PC12 cells via reducing ROS production[J]. Evid Based Complement Alternat Med, 2015:189-239
Abstract Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic (DA) neurons at the substantia nigra. Mitochondrial dysfunction and inflammatory responses are involved in the mechanism of cell damage in PD. 6-Hydroxydopamine (6-OHDA), a dopamine analog, specifically damages dopaminergic neurons. Echinacoside (ECH) is a phenylethanoid glycoside isolated from the stems of Cistanche salsa, showing a variety of neuroprotective effects in previous studies. The present study was to investigate its effect against 6-OHDA-induced neurotoxicity and possible mechanisms in PC12 cells. The results showed that 6-OHDA reduced cell viability, decreased oxidation-reduction activity, decreased mitochondrial membrane potential, and induced mitochondria-mediated apoptosis compared with untreated PC12 cells. However, echinacoside treatment significantly attenuated these changes induced by 6-OHDA. In addition, echinacoside also could significantly alleviate the inflammatory responses induced by 6-OHDA. Further research showed that echinacoside could reduce 6-OHDA-induced ROS production in PC12 cells. These results suggest that the underlying mechanism of echinacoside against 6-OHDA-induced neurotoxicity may be involve in attenuating mitochondrial dysfunction and inflammatory responses by reducing ROS production.
ZHAOQ, GAOJ, LIW, et al.Neurotrophic and neurorescue effects of Echinacoside in the subacute MPTP mouse model of Parkinson’s disease[J]. Brain Res, 2010, 1346(1): 224-236.
Many experiments support the notion that augmentation of neurotrophic factors' (NTFs) activity, especially glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) could prevent or halt the progress of neurodegeneration in Parkinson's disease (PD). However, application of NTFs as therapeutic agents for PD is hampered by the difficulty in delivering them to...
WU CR, LIN HC, SU MH.Reversal by aqueous extracts of cistanche tubulosa from behavioral deficits in Alzheimer’s disease-like rat model: relevance for amyloid deposition and central neurotransmitter function[J]. BMC Complement Altern Med, 2014, 14(1):1-11.
Cistanche tubulosa (Schenk) R. Wight (CT) is commonly used to treat forgetfulness by traditional Chinese physicians. This study presents the ameliorating effects of CT extract which was quantified with three phenylpropanoid glycosides in Alzheimer’s disease (AD)-like rat model. Amyloid β peptide 1-42 (Aβ 1-42) intracisternally infused to rats by osmotic pump (Alzet 2002) was used as an AD-like rat model. The major pathological makers were measured including Aβ 1-42 immunohistochemical stain, behavioral tests (inhibitory avoidance task and Morris water maze) and central neurotransmitter functions. Aβ 1-42 caused the cognitive deficits, the increase in the amyloid deposition and acetylcholinesterase activities, and the decrease in the levels of brain’s acetylcholine and dopamine. Daily administration of CT extract throughout Aβ 1-42 infusion periods ameliorated the cognitive deficits, decreased amyloid deposition and reversed cholinergic and hippocampal dopaminergic dysfunction caused by Aβ 1-42. Donepezil also ameliorated the cognitive dysfunction, but only blocked the amyloid deposition and cholinergic dysfunction caused by Aβ 1-42. We suggest that CT extract, containing enough echinacoside and acteoside, ameliorated the cognitive dysfunction caused by Aβ 1-42 via blocking amyloid deposition, reversing cholinergic and hippocampal dopaminergic neuronal function.
SPERONIE, GOVONIP, GUIZZARDIS, et al.Anti-inflammatory and cicatrizing activity of Echinacea pallida Nutt root extract[J]. J Ethnopharmacol, 2002, 79(2): 265-272.
Among the different species belonging to the Echinacea family, largely used in traditional medicine, Echinacea pallida, Echinacea purpurea and Echinacea angustifolia were investigated. These different species, due to their difficult identification, were commonly confused in the past and probably used indifferently for the same therapeutic purposes. In fact, the three species have in common, some pharmacological activities, based on the presence of active compounds that act additively and synergistically. Nevertheless, the composition of each species has slight variation in the amount of each active component. In particular, echinacoside, a caffeoyl derivative, is present in E. pallida and only in traces in E. angustifolia. It seems to have protective effects on skin connective tissue and to enhance wound healing. The anti-inflammatory and wound healing activities of echinacoside, compared with the ones of the total root extract of E. pallida and E. angustifolia, were examined in rats, after topical application. The tissues of the treated animals were evaluated after 24, 48 and 72 h treatment and excised for histological observation at the end of the experiment. Results confirm the good anti-inflammatory and wound healing properties of E. pallida and of its constituent echinacoside, with respect to E. purpurea and control. This activity probably resides in the antihyaluronidase activity of echinacoside.
JIAY, GUANQ, JIANGY, et al.Amelioration of dextran sulphate sodium-induced colitis in mice by echinacoside-enriched extract of Cistanche tubulosa[J]. Phytother Res, 2014, 28(1): 110-119.
Echinacoside (ECH) is a major bioactive phenyethanoids in medicinal herba and has been reported to have antiinflammatory activity and beneficial effect on wound healing in many experimental studies. This study was to test the efficacy of ECH‐enriched extract of in the treatment of dextran sulphate sodium (DSS)‐induced colitis, a preclinical model of ulcerative colitis. Oral administration of ECH extract significantly suppresses the development of acute colitis, indicated by lowering disease activity index (65<650.0001, 65=658) and preventing colonic damage (65=650.0336). Histological examinations showed that ECH extract treatment protected intestinal epithelium from inflammatory injury (65=650.0249) but had less effect on inflammatory cellular infiltration (65=650.1753). The beneficial effect of ECH extract treatment was associated with upregulation of transforming growth factor (TGF)‐β1 as well as with an increase in the number of Ki67proliferating cells in diseased colons (65<650.0001). In cultured MODE‐K cells, the addition of ECH extract enhanced wound healing that depended on TGF‐β1 expression. These data suggest that ECH extract possesses a greater efficacy in preventing DSS‐induced colitis in mice, implying the potential of ECH or its derivatives for clinically treating inflammatory bowel disease. Copyright 08 2013 John Wiley & Sons, Ltd.
BOUMAG, STROBERW.The immunological and genetic basis of inflammatory bowel disease[J]. Nat Rev Immunol, 2003, 3(7): 521-533.
The inflammatory bowel diseases (IBDs), Crohn's disease and ulcerative colitis, are chronic inflammatory disorders of the gastrointestinal tract. Enormous progress has been made recently in understanding the pathogenesis of these diseases. Through the study of patients and mouse models, it has emerged that Crohn's disease is driven by the production of interleukin-12 (IL-12) and interferon-gamma (IFN-gamma), whereas ulcerative colitis is probably driven by the production of IL-13. A second area of progress is in the identification of specific genetic abnormalities that are responsible for disease. The most important finding is the identification of mutations in the gene that encodes NOD2 (nucleotide-binding oligomerization domain 2) protein in a subgroup of patients with Crohn's disease. Here, we discuss these recent findings and the implications for therapy.
BOIRIVANTM, FUSS IJ, CHUA, et al.Oxazolone colitis: a murine model of T helper cell type 2 colitis treatable with antibodies to interleukin 4[J]. J Exp Med, 1998, 188(10): 1929-1939.
Abstract In this study we describe oxazolone colitis, a new form of experimental colitis. This model is induced in SJL/J mice by the rectal instillation of the haptenating agent, oxazolone, and is characterized by a rapidly developing colitis confined to the distal half of the colon; it consists of a mixed neutrophil/lymphocyte infiltration limited to the superficial layer of the mucosa which is associated with ulceration. Oxazolone colitis is a T helper cell type 2 (Th2)-mediated process since stimulated T cells from lesional tissue produce markedly increased amounts of interleukin (IL)-4 and IL-5; in addition, anti-IL-4 administration leads to a striking amelioration of disease, whereas anti-IL-12 administration either has no effect or exacerbates disease. Finally, this proinflammatory Th2 cytokine response is counterbalanced by a massive transforming growth factor-beta (TGF-beta) response which limits both the extent and duration of disease: lesional (distal) T cells manifest a 20-30-fold increase in TGF-beta production, whereas nonlesional (proximal) T cells manifest an even greater 40-50-fold increase. In addition, anti-TGF-beta administration leads to more severe inflammation which now involves the entire colon. The histologic features and distribution of oxazolone colitis have characteristics that resemble ulcerative colitis (UC) and thus sharply distinguish this model from most other models, which usually resemble Crohn's disease. This feature of oxazolone colitis as well as its cytokine profile have important implications to the pathogenesis and treatment of UC.
ROUSSEAUB, TATEYAI, LIMX, et al.Investigation of anti-hyaluronidase treatment on vocal fold wound healing[J]. J Voice, 2006, 20(3): 443-451.
Clinical and pathohistological studies on the 44 cases with hepatitis or cirrhosis of the liver histologically confirmed by biopsy except 5 cases, who developed hepatoma in variable periods of time of follow-up, were reported.The prevalence of HBsAg in their sera was 35.7% and that of anti-HBc was 67.4%. All cases whose sera were positive for HBsAg at death showed positive HBsAg in the liver obtained by biopsy on the first occasion. This indicated that they had persistent infection of HBV.Retrospective studies suggested that HBsAg positive, latent cirrhosis appeared to have a higher risk to develop hepatoma. Frequent determination of serum AFP could not be a clue for the early detection of the hepatoma so far in cases reported. In the biopsied liver of a case with chronic active hepatitis was found a minimal deviation hepatoma 4 years befbre the full-development of hepatoma. This finding suggested that hepatoma with cirrhosis might develop in some cases already in a stage of chronic hepatitis.
LIX, GOUC, YANGH, et al.Echinacoside ameliorates D-galactosamine plus lipopolysaccharide-induced acute liver injury in mice via inhibition of apoptosis and inflammation[J]. Scand J Gastroenterol, 2014, 49(8): 993-1000.
This study aimed to investigate the protective effects of echinacoside, one of the phenylethanoids isolated from the stems of Cistanche salsa, a Chinese herbal medicine, on D-galactosamine (GalN) and lipopolysaccharide (LPS)-induced acute liver injury in mice.We administered GalN (650 mg/kg) together with LPS (30 g/kg) to mice by intraperitoneal injection to induce acute liver damage. Echinacoside (60 mg/kg) was given intraperitoneally to mice at 1 h prior to GalN/LPS exposure. Mice were sacrificed at different time points following GalN/LPS treatment, and the liver and blood samples were collected for future analysis.It showed that GalN/LPS treatment produced severe hepatic injury, evidenced by significantly elevated plasma alanine aminotransferase (ALT) levels and abnormal histological changes such as hepatocyte necrosis or apoptosis, hemorrhage, fatty degeneration, and neutrophil infiltration. Notably, pretreatment with echinacoside remarkably improved the survival rate of GalN/LPS-treated mice and attenuated acute hepatotoxicity, as demonstrated by decreased ALT levels and improved histological signs. Echinacoside shows both anti-apoptotic and anti-inflammatory properties, characterized by a substantial inhibition of hepatocyte apoptosis and a significant reduction in the inflammatory markers, including myeloperoxidase, extracellular nucleosomes, high-mobility group box 1, and inflammatory cytokines in the plasma of mice, which may be important mechanisms related to its protective effect.Our results suggest that echinacoside can provide a pronounced protection against GalN/LPS-induced acute liver injury in mice, which may complement the available strategies for management of acute liver damage in clinical settings.
MORIKAWAT, PANY, NINOMIYAK, et al.Acylated phenylethanoid oligoglycosides with hepatoprotective activity from the desert plant Cistanche tubulosa[J]. Bioorg Med Chem, 2010, 18(5): 1882-1890.
The methanolic extract from fresh stems of Cistanche tubulosa (Orobanchaceae) was found to show hepatoprotective effects against d -galactosamine ( d -GalN)/lipopolysaccharide (LPS)-induced liver injury in mice. From the extract, three new phenylethanoid oligoglycosides, kankanosides H 1 ( 1 ), H 2 ( 2 ), and I ( 3 ), were isolated together with 16 phenylethanoid glycosides ( 4 – 19 ) and two acylated oligosugars ( 20 , 21 ). The structures of 1 – 3 were determined on the basis of spectroscopic properties as well as of chemical evidence. Among the isolates, echinacoside ( 4 , IC 50 02=0210.202μM), acteoside ( 5 , 4.602μM), isoacteoside ( 6 , 5.302μM), 2′-acetylacteoside ( 8 , 4.802μM), and tubuloside A ( 10 , 8.602μM) inhibited d -GalN-induced death of hepatocytes. These five isolates, 4 (31.102μM), 5 (17.802μM), 6 (22.702μM), 8 (25.702μM), and 10 (23.202μM), and cistantubuloside B 1 ( 11 , 21.402μM) also reduced TNF-α-induced cytotoxicity in L929 cells. Moreover, principal constituents ( 4 – 6 ) exhibited in vivo hepatoprotective effects at doses of 25–10002mg/kg, po.
LIF, YANGX, YANGY, et al.Antiosteoporotic activity of echinacoside in ovariectomized rats[J]. Phytomedicine, 2013, 20(6): 549-557.
Abstract PURPOSE: Echinacoside (ECH), isolated from Cistanche tubulosa (Schrenk) R. Wight stems, has been reported to enhance bone regeneration in MC3T3-E1 cells in vitro. The objectives of this study were to investigate the antiosteoporotic effect of ECH on bone metabolism in the ovariectomized (OVX) rat model of osteoporosis in vivo. METHODS: Fifty-six aged 6 months female Sprague-Dawley rats were randomly assigned into sham-operated group (SHAM) and six OVX subgroups (n=8 each). The OVX rats were then subdivided into six groups treated with vehicle (OVX), Xian-ling-gu-bao (XLGB, 0.5 g/kg body weight/day, orally), 17尾-estradiol (E2, 50 g/kg body weight/day, orally) or ECH (30, 90, and 270 mg/kg body weight, daily, orally) for 12 weeks respectively. We evaluated the pharmacological effects of E2, XLGB and ECH against osteoporosis by evaluating the body weight, uterus wet weight, serum and urine biochemical parameters, bone mineral density (BMD), bone biomechanical properties, bone microarchitecture, bone histomorphology and uterus immunohistochemistry. RESULTS: In OVX rats, the increases of body weight, serum hydroxyproline (HOP) levels, and the decreases of uterus wet weight and BMD were significantly reversed by ECH treatment. Moreover, three dosages of ECH completely corrected the increased urine concentration of calcium (Ca), inorganic phosphorus (P), and HOP observed in OVX rats. Furthermore, Micro-CT analysis results of distal femur showed that all ECH-treated groups notably enhanced bone quality compared to OVX group (p<0.05). Consistent with this finding, total femur BMD and biomechanical strength of tibia were significantly improved (p<0.05) after 12 weeks ECH administration. Histological results also showed the protective activity of ECH through promotion of bone formation and suppression of bone resorption. In addition, the ECH administration also significantly enhanced the expression of ER in the uteri according to immunohistochemical evaluation (p<0.05). Those findings, based on the serum and urine biochemical, BMD, Micro-CT, biomechanical test, histopathological and immunohistochemical parameters, showed that ECH has a notable antiosteoporotic effect, similar to estrogen, especially effective for prevention osteoporosis induced by estrogen deficiency. CONCLUSION: These results suggest that ECH, as a new class of phytoestrogen, has a remarkable antiosteoporotic activity, and may be a promising candidate for treatment of postmenopausal osteoporosis induced by estrogen deficiency in a natural way through herbal resources. Copyright 漏 2013 Elsevier GmbH. All rights reserved.
LIF, YANGY, ZHUP, et al.Echinacoside promotes bone regeneration by increasing OPG/RANKL ratio in MC3T3-E1 cells[J]. Fitoterapia, 2012, 83(8): 1443-1450.
Echinacoside (ECH), isolated from Cistanche tubulosa (Schrenk) R. Wight stems, was subjected to in vitro experiments to investigate its bioactivities on proliferation, differentiation and mineralization of the osteoblastic cell line MC3T3-E1. MTT assay, the alkaline phosphatase (ALP) activity and calcium deposition were determined, and the secretion of collagen I (COL I), osteocalcin (OCN), osteoprotegerin (OPG) and receptor activator of nuclear factor-魏B ligand (RANKL) were also assayed by enzyme-linked immunosorbent assay (ELISA). The results showed that ECH caused a significant increase in cell proliferation, ALP activity, COL I contents, OCN levels and an enhancement of mineralization in osteoblasts at the concentration range from 0.01 to 10nmol路L(-1) (p<0.05), suggesting that ECH has a stimulatory effect on osteoblastic bone formation or has potential activity against osteoporosis. In addition, the ratio of OPG/RANKL also could be enhanced by ECH. These findings provide the potent evidence that ECH can promote bone regeneration in cultured osteoblastic MC3T3-E1 cells, which might be done by elevating the OPG/RANKL ratio, and potential evidence for echinacoside to be a promising drug or a lead compound in the development of disease-modifying drug to prevent osteoporosis.
YANGX, LIF, YANGY, et al.Efficacy and safety of echinacoside in a rat osteopenia model[J]. Evid Based Complement Alternat Med, 2013, 2013(4): 926-928.
This study aimed to investigate the efficacy and safety of echinacoside (ECH) using an osteopenia rat model. Forty-eight 6-month-old female Sprague-Dawley rats were randomly divided into one sham-operated group (SHAM) and five OVX (ovariectomized) subgroups: SHAM with vehicle 0.5% carboxymethylcellulose sodium (0.5% CMC-Na) and OVX with vehicle (OVX), OVX with 17 尾 -estradiol (E2), and OVX with ECH of graded doses (ECH-L, ECH-M, and ECH-H). The effects of ECH and E2 on serum biochemical parameters, bone mineral density (BMD), bone biomechanical properties, bone microarchitecture, and immunohistochemistry were examined, and safety assessments were also evaluated. The results showed that ECH treatments improved total femur BMD, bone microarchitecture, and biomechanical properties and decreased serum marker levels in comparison to OVX group. Moreover, ECH administration significantly increased osteoprotegerin (OPG) level, and decreased receptor activator of nuclear factor- 魏 B ligand (RANKL) level in serum, as well as in proximal femur. Importantly, ECH treatment ameliorated the lipid parameters without the overall incidences of adverse events of uterus and mammary gland compared to OVX and SHAM groups. This study demonstrated that administration of ECH for 12 weeks can effectively and safely prevent OVX-induced osteoporosis in rats via increasing the OPG/RANKL ratio.
RAIP, ONDER TT, YOUNG JJ, et al.Continuous elimination of oxidized nucleotides is necessary to prevent rapid onset of cellular senescence[J]. Proc Natl Acad Sci USA, 2009, 106(1): 169-174.
Abstract Reactive oxygen species (ROS) appear to play a role in limiting both cellular and organismic lifespan. However, because of their pleiotropic effects, it has been difficult to ascribe a specific role to ROS in initiating the process of cellular senescence. We have studied the effects of oxidative DNA damage on cell proliferation, believing that such damage is of central importance to triggering senescence. To do so, we devised a strategy to decouple levels of 8-oxoguanine, a major oxidative DNA lesion, from ROS levels. Suppression of MTH1 expression, which hydrolyzes 8-oxo-dGTP, was accompanied by increased total cellular 8-oxoguanine levels and caused early-passage primary and telomerase-immortalized human skin fibroblasts to rapidly undergo senescence, doing so without altering cellular ROS levels. This senescent phenotype recapitulated several salient features of replicative senescence, notably the presence of senescence-associated beta-galactosidase (SA beta-gal) activity, apparently irreparable genomic DNA breaks, and elevation of p21(Cip1), p53, and p16(INK4A) tumor suppressor protein levels. Culturing cells under low oxygen tension (3%) largely prevented the shMTH1-dependent senescent phenotype. These results indicate that the nucleotide pool is a critical target of intracellular ROS and that oxidized nucleotides, unless continuously eliminated, can rapidly induce cell senescence through signaling pathways very similar to those activated during replicative senescence.
SANTOS MA, GUTIERREZ-MARTINEZP, CHEN HT, et al.DNA-damage-induced differentiation of leukaemic cells as an anti-cancer barrier[J]. Nature, 2014, 514(7520): 107-111.
ABSTRACT Self-renewal is the hallmark feature both of normal stem cells and cancer stem cells. Since the regenerative capacity of normal haematopoietic stem cells is limited by the accumulation of reactive oxygen species and DNA double-strand breaks, we speculated that DNA damage might also constrain leukaemic self-renewal and malignant haematopoiesis. Here we show that the histone methyl-transferase MLL4, a suppressor of B-cell lymphoma, is required for stem-cell activity and an aggressive form of acute myeloid leukaemia harbouring the MLL-AF9 oncogene. Deletion of MLL4 enhances myelopoiesis and myeloid differentiation of leukaemic blasts, which protects mice from death related to acute myeloid leukaemia. MLL4 exerts its function by regulating transcriptional programs associated with the antioxidant response. Addition of reactive oxygen species scavengers or ectopic expression of FOXO3 protects MLL4(-/-) MLL-AF9 cells from DNA damage and inhibits myeloid maturation. Similar to MLL4 deficiency, loss of ATM or BRCA1 sensitizes transformed cells to differentiation, suggesting that myeloid differentiation is promoted by loss of genome integrity. Indeed, we show that restriction-enzyme-induced double-strand breaks are sufficient to induce differentiation of MLL-AF9 blasts, which requires cyclin-dependent kinase inhibitor p21(Cip1) (Cdkn1a) activity. In summary, we have uncovered an unexpected tumour-promoting role of genome guardians in enforcing the oncogene-induced differentiation blockade in acute myeloid leukaemia.
HARRIS IS, BRUSTLEA, MOLYNEUX SD, et al.Glutathione and thioredoxin antioxidant pathways synergize to drive cancer initiation and progression[J]. Cancer Cell, 2015, 27(2): 211-222.
Controversy over the role of antioxidants in cancer has persisted for decades. Here, we demonstrate that synthesis of the antioxidant glutathione (GSH), driven by GCLM, is required for cancer initiation. Genetic loss of Gclm prevents a tumor鈥檚 ability to drive malignant transformation. Intriguingly, these findings canbe replicated using an inhibitor of GSH synthesis, but only if delivered prior to cancer onset, suggesting that at later stages of tumor progression GSH becomes dispensable potentially due to compensation from alternative antioxidant pathways. Remarkably, combined inhibition of GSH and thioredoxin antioxidant pathways leads to a synergistic cancer cell death invitro and invivo, demonstrating theimportance of these two antioxidants to tumor progression and as potential targets for therapeutic intervention.
DONGL, YUD, WUN, et al.Echinacoside induces apoptosis in human SW480 colorectal cancer cells by induction of oxidative DNA damages[J]. Int J Mol Sci, 2015, 16(7): 14655-14668.
Echinacoside is a natural compound with potent reactive oxygen species (ROS)-scavenging and anti-oxidative bioactivities, which protect cells from oxidative damages. As cancer cells are often under intense oxidative stress, we therefore tested if Echinacoside treatment would promote cancer development. Surprisingly, we found that Echinacoside significantly inhibited the growth and proliferation of a panel of cancer cell lines. Treatment of the human SW480 cancer cells with Echinacoside resulted in marked apoptosis and cell cycle arrest, together with a significant increase in active caspase 3 and cleaved PARP, and upregulation of the G1/S-CDK blocker CDKN1B (p21). Interestingly, immunocytochemistry examination of drug-treated cancer cells revealed that Echinacoside caused a significant increase of intracellular oxidized guanine, 8-oxoG, and dramatic upregulation of the double-strand DNA break (DSB)-binding protein 53BP1, suggesting that Echinacoside induced cell cycle arrest and apoptosis in SW480 cancer cells via induction of oxidative DNA damages. These results establish Echinacoside as a novel chemical scaffold for development of anticancer drugs.
DONGL, WANGH, NIUJ, et al.Echinacoside induces apoptotic cancer cell death by inhibiting the nucleotide pool sanitizing enzyme MTH1[J]. Onco Targets Ther, 2015(8): 3649-3664.
Abstract: Inhibition of the nucleotide pool sanitizing enzyme MTH1 causes extensive oxidative DNA damages and apoptosis in cancer cells and hence may be used as an anticancer strategy. As natural products have been a rich source of medicinal chemicals, in the present study, we used the MTH1-catalyzed enzymatic reaction as a high-throughput in vitro screening assay to search for natural compounds capable of inhibiting MTH1. Echinacoside, a compound derived from the medicinal plants Cistanche and Echinacea, effectively inhibited the catalytic activity of MTH1 in an in vitro assay. Treatment of various human cancer cell lines with Echinacoside resulted in a significant increase in the cellular level of oxidized guanine (8-oxoguanine), while cellular reactive oxygen species level remained unchanged, indicating that Echinacoside also inhibited the activity of cellular MTH1. Consequently, Echinacoside treatment induced an immediate and dramatic increase in DNA damage markers and upregulation of the G1/S-CDK inhibitor p21, which were followed by marked apoptotic cell death and cell cycle arrest in cancer but not in noncancer cells. Taken together, these studies identified a natural compound as an MTH1 inhibitor and suggest that natural products can be an important source of anticancer agents.
WANGS, ZHENGG, TIANS, et al.Echinacoside improves hematopoietic function in 5-FU-induced myelosuppression mice[J]. Life Sci, 2015, 123(1): 86-92.
ECH could improve the hematopoietic function of bone marrow in 5-FU-induced myelosuppression mice. ECH can be considered as an alternative effective therapy for patients during chemotherapy or HSC transplantation.
SENCHINA DS, STRAUCH JH, HOFFMANN GB, et al.Phytochemical and immunomodulatory properties of an Echinacea laevigata (Asteraceae) tincture[J]. J Altern Complement Med, 2011, 17(4): 375-377.
Echinacea preparations are consumed for the prevention or treatment of upper respiratory infections.The objective of this study was to provide the first data regarding the in vitro immunomodulatory properties of the American federally endangered species Echinacea laevigata (Asteraceae).Human peripheral blood mononuclear cells were cultured with root tinctures from E. laevigata, E. angustifolia, E. pallida, and E. purpurea. Cytokine production (tumor necrosis factor [TNF], interleukin [IL]-2, IL-10) and mononuclear cell proliferation were measured. High-performance liquid chromatography was used to assay levels of known bioactive compounds from all extracts tested to statistically determine whether there were relationships between extract phytochemical content and observed immune effects.E. laevigata extract was most similar to E. pallida extract and able to augment IL-10 and mononuclear cell proliferation, but not TNF or IL-2. Echinacoside, a caffeic acid derivative, correlated most strongly with results.This species may deserve continued investigation in both experimental and therapeutic contexts.
MORIKAWAT, NINOMIYAK, IMAMURAM, et al.Acylated phenylethanoid glycosides, echinacoside and acteoside from Cistanche tubulosa, improve glucose tolerance in mice[J]. J Nat Med, 2014, 68(3): 561-566.
Acylated phenylethanoid glycosides, echinacoside (1) and acteoside (2), principal constituents in stems of Cistanche tubulosa (Orobanchaceae), inhibited the increase in postprandial blood glucose levels in starch-loaded mice at doses of 250-50002mg/kg p.o. These compounds (1 and 2) also significantly improved glucose tolerance in starch-loaded mice after 202weeks of continuous administration at doses of 125 and/or 25002mg/kg/day p.o. without producing significant changes in body weight or food intake. In addition, several constituents from C. tubulosa, including 1 (IC5002=023.102μM), 2 (1.202μM), isoacteoside (3, 4.602μM), 2'-acetylacteoside (4, 0.07102μM), tubulosides A (5, 8.802μM) and B (9, 4.002μM), syringalide A 3-O-α-L-rhamnopyranoside (10, 1.102μM), campneoside I (13, 0.5302μM), and kankanoside J1 (14, 9.302μM), demonstrated potent rat lens aldose reductase inhibitory activity. In particular, the potency of compound 4 was similar to that of epalrestat (0.07202μM), a clinical aldose reductase inhibitor.
WANGY, HAOH, WANGG, et al.An approach to identifying sequential metabolites of a typical phenylethanoid glycoside, echinacoside, based on liquid chromatography-ion trap-time of flight mass spectrometry analysis[J]. Talanta, 2009, 80(2): 572-580.
Metabolite identification for the compounds that undergo multiple and sequential metabolism is still a great challenge. Echinacoside (ECH), a typical phenylethanoid , contains multiple unstable chemical bonds and high reactive functional groups which are susceptible to multiple pathways of degradation and metabolism, leading great difficulties for its metabolite identification. This study proposed a novel approach for rapidly identifying the complicated and unpredictable metabolites of ECH, based on the powerful liquid chromatography hybrid ion trap and time of flight mass spectrometry (LC/MS-IT-TOF) analysis. Four degradation products were rapidly identified via the "fragmentation-degradation" comparisons. Five phase I and phase II metabolites of the degradation products were rapidly characterized via the crossover mass differences comparisons of their quasi-with the potential precursors. Four direct phase I and phase II metabolites of the parent compound were identified by the mass differences analysis of the between metabolites and the parent compound. Multiple stages of fragmentation patterns were used to confirm the metabolites characterizations. This study provides a novel approach to characterizing the complicated metabolites, and would be widely applicable for the metabolite identification of .
YANGH, WANGG, HAOH, et al.A sensitive and specific liquid chromatography/tandem mass spectrometry method for determination of echinacoside and its pharmacokinetic application in rats[J]. Biomed Chromatogr, 2009, 23(6): 630-637.
ABSTRACT A rapid and sensitive method based on liquid chromatography/tandem mass spectrometry (LC/MS/MS) for the determination of echinacoside in rat plasma was established and fully validated. A single step of liquid-liquid extraction with n-butanol was utilized. Chromatographic separation of the analyte and the internal standard (IS), chlorogenic acid, from the sample matrix was performed using a Capcell-MG C(18) analytical column (100 2.0 mm x 5 microm), with a gradient of acetonitrile and water containing 0.1% acetic acid as the mobile phase. Detection was performed on a triple quadrupole tandem mass spectrometer equipped with electrospray ionization source operated in negative ion selected reaction monitoring mode. The method was linear in the concentration range 10-2500 ng/mL. The deviations of both intra- and inter-day precisions (RSD) were 7.1% and the assay accuracies were within 99.2-106.5%. Echinacoside proved to be stable during sample storage, preparation and analysis when an antioxidant solution was used. The method was successfully applied to a pharmacokinetic study in rats after an intragastric administration of echinacoside (100 mg/kg). With the lower limit of quantification at 10 ng/mL, this method proved to have sufficient selectivity, sensitivity and reproducibility for the pharmacokinetic study of echinacoside.
SHEN JY, YANG XL, YANG ZL, et al.Enhancement of absorption and bioavailability of echinacoside by verapamil or clove oil [J ]. Drug Des Devel Ther, 2015(9): 4685-4693.
This present study investigated the absorption kinetics of echinacoside (ECH) in situ and in vitro and its oral bioavailability in rats. Additional aim was to find an agent(s) to promote ECH absorption and oral bioavailability among two efflux proteins and three absorption promoters.ECH absorption behaviors were investigated by everted gut sac model in vitro and single-pass intestinal perfusion model in situ. Pharmacokinetics study was performed to investigate the influences of verapamil and clove oil on ECH bioavailability in vivo. All samples were measured at different time intervals by high performance liquid chromatography.The results showed that the effective permeability coefficient (P eff) and apparent permeability coefficient of ECH were 0.8310(-6)-3.2310(-6) cm/s and 2.9910(-6)-9.8610(-6) cm/s, respectively. The P eff among duodenum, jejunum, and ileum were not statistically different, but they were higher than colon (P<0.01), which demonstrated that intestinal ECH absorption was poor and site dependent. Additionally, verapamil and clove oil significantly increased the jejunal P eff of ECH both in situ and in vitro. Moreover, the bioavailability of ECH in combination with verapamil and clove oil were increased by 1.37-fold (P<0.05) and 2.36-fold (P<0.001), respectively, when compared to ECH group. Overall, verapamil and clove oil facilitated ECH absorption and oral bioavailability.The absorption and bioavailability of ECH were enhanced by verapamil and clove oil, respectively, both in vitro and in vivo. Consequently, the combination of verapamil and clove oil with ECH will be a promising and effective approach to promote intestinal absorption and oral bioavailability of ECH.
JIAC, SHIH, WUX, et al.Determination of echinacoside in rat serum by reversed-phase high-performance liquid chromatography with ultraviolet detection and its application to pharmacokinetics and bioavailability[J]. J Chromatogr B Analyt Technol Biomed Life Sci, 2006, 844(2): 308-313.
ABSTRACT A rapid and simple high-performance liquid chromatographic (HPLC) method has been developed and validated for the determination of echinacoside (ECH) in rat serum. After protein precipitation of serum sample with trichloroacetic acid, the supernatant was directly injected and analyzed on a C(18) CapcellACR analytical column (150 mm x 4.6mm I.D. 5 microm) with a mobile phase consisting of acetonitrile-0.5% acetic acid (15.5:84.5, v/v). The UV detector was set at 330 nm. The lower limit of detection and quantification were 9 and 29.2 ng/mL, respectively, and the calibration curves were linear over the concentration range of 29.2-18250 ng/mL. The assay method was successfully applied to the study of the pharmacokinetics and bioavailability of ECH in rat.
JIA CQ, SHI HM, JINW, et al.Metabolism of echinacoside, a good antioxidant, in rats: isolation and identification of its biliary metabolites[J]. Drug Metab Dispos, 2009, 37(2):431-438.
Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
Reversal by aqueous extracts of cistanche tubulosa from behavioral deficits in Alzheimer’s disease-like rat model: relevance for amyloid deposition and central neurotransmitter function
Antiosteoporotic activity of echinacoside in ovariectomized rats
1
2013
... 骨质疏松症是发病率较高的骨疾病,尤其是绝经后妇女.松果菊苷具有雌激素样作用,对骨质疏松,尤其是雌激素降低引起的骨质疏松具有良好疗效.LI等[28]通过切除卵巢建立大鼠骨质疏松模型,用松果菊苷处理后,大鼠尿中钙磷显著下降,骨矿物密度(bone mineral density, BMD)升高,大鼠骨质增多,并且增加了骨形成和降低了骨吸收,对大鼠雌激素缺乏引起的骨质疏松有较好的治疗作用.松果菊苷还能够促进细胞增殖、提高碱性磷酸酶(alkaline phosphatase,ALP)水平、升高胶原蛋白-1(collagen I, COL I)和骨钙蛋白(osteocalcin, OCN)浓度,能有效刺激骨形成,对抗骨质疏松[29].另外,YANG等[30]也提出,松果菊苷可以改善模型鼠股骨的BMD和骨微结构,增加骨保护素(osteoprotegerin, OPG)的水平,降低核因子受体激活因子配体(receptor activator of nuclear factor-κB ligand, RANKL)水平,对雌激素缺乏引起的骨质疏松有良好疗效.雌激素治疗盆底功能障碍性疾病一直存在争议,主要在于雌激素副作用较多,但是植物雌激素副作用少且轻,松果菊苷应用于妇科疾病值得期待. ...
Echinacoside promotes bone regeneration by increasing OPG/RANKL ratio in MC3T3-E1 cells
1
2012
... 骨质疏松症是发病率较高的骨疾病,尤其是绝经后妇女.松果菊苷具有雌激素样作用,对骨质疏松,尤其是雌激素降低引起的骨质疏松具有良好疗效.LI等[28]通过切除卵巢建立大鼠骨质疏松模型,用松果菊苷处理后,大鼠尿中钙磷显著下降,骨矿物密度(bone mineral density, BMD)升高,大鼠骨质增多,并且增加了骨形成和降低了骨吸收,对大鼠雌激素缺乏引起的骨质疏松有较好的治疗作用.松果菊苷还能够促进细胞增殖、提高碱性磷酸酶(alkaline phosphatase,ALP)水平、升高胶原蛋白-1(collagen I, COL I)和骨钙蛋白(osteocalcin, OCN)浓度,能有效刺激骨形成,对抗骨质疏松[29].另外,YANG等[30]也提出,松果菊苷可以改善模型鼠股骨的BMD和骨微结构,增加骨保护素(osteoprotegerin, OPG)的水平,降低核因子受体激活因子配体(receptor activator of nuclear factor-κB ligand, RANKL)水平,对雌激素缺乏引起的骨质疏松有良好疗效.雌激素治疗盆底功能障碍性疾病一直存在争议,主要在于雌激素副作用较多,但是植物雌激素副作用少且轻,松果菊苷应用于妇科疾病值得期待. ...
Efficacy and safety of echinacoside in a rat osteopenia model
1
2013
... 骨质疏松症是发病率较高的骨疾病,尤其是绝经后妇女.松果菊苷具有雌激素样作用,对骨质疏松,尤其是雌激素降低引起的骨质疏松具有良好疗效.LI等[28]通过切除卵巢建立大鼠骨质疏松模型,用松果菊苷处理后,大鼠尿中钙磷显著下降,骨矿物密度(bone mineral density, BMD)升高,大鼠骨质增多,并且增加了骨形成和降低了骨吸收,对大鼠雌激素缺乏引起的骨质疏松有较好的治疗作用.松果菊苷还能够促进细胞增殖、提高碱性磷酸酶(alkaline phosphatase,ALP)水平、升高胶原蛋白-1(collagen I, COL I)和骨钙蛋白(osteocalcin, OCN)浓度,能有效刺激骨形成,对抗骨质疏松[29].另外,YANG等[30]也提出,松果菊苷可以改善模型鼠股骨的BMD和骨微结构,增加骨保护素(osteoprotegerin, OPG)的水平,降低核因子受体激活因子配体(receptor activator of nuclear factor-κB ligand, RANKL)水平,对雌激素缺乏引起的骨质疏松有良好疗效.雌激素治疗盆底功能障碍性疾病一直存在争议,主要在于雌激素副作用较多,但是植物雌激素副作用少且轻,松果菊苷应用于妇科疾病值得期待. ...
Continuous elimination of oxidized nucleotides is necessary to prevent rapid onset of cellular senescence
An approach to identifying sequential metabolites of a typical phenylethanoid glycoside, echinacoside, based on liquid chromatography-ion trap-time of flight mass spectrometry analysis
A sensitive and specific liquid chromatography/tandem mass spectrometry method for determination of echinacoside and its pharmacokinetic application in rats
Determination of echinacoside in rat serum by reversed-phase high-performance liquid chromatography with ultraviolet detection and its application to pharmacokinetics and bioavailability
, 洪莉
