| 薛冬英,洪嘉禾,徐列明.丹参酚酸B对转化生长因子β1和血小板衍生生长因子-BB在肝星状细胞内信号传导的影响[J].中国中西医结合杂志,2006,(5):439-442 |
| 丹参酚酸B对转化生长因子β1和血小板衍生生长因子-BB在肝星状细胞内信号传导的影响 |
| Effects of Salvianolic Acid B on Signal Transduction Induced by Transforming Growth Factor-BB and Platelet-derived Growth Factor-β1 in Hepatic Stellate Cells of Rats |
| 免费下载全文 查看/发表评论 下载PDF阅读器 |
| |
| DOI： |
| 中文关键词: 肝纤维化 丹参酚酸B 细胞内信号传导 肝星状细胞 转化生长因子β1 血小板衍生生长因子-BB |
| 英文关键词:liver fibrosis salvianolic acid B intracellular signal transduction hepatic stellate cell transforming growth factor-β1 platelet-derived growth factor-BB |
| 基金项目:国家自然科学基金项目(No.30271657);上海市重点学科建设项目资助(No.Y0302);上海市教委重点学科建设项目资助 |
|
| 摘要点击次数: 1499 |
| 全文下载次数: 2 |
| 中文摘要: |
| 目的探讨丹参酚酸B(SA-B)抗肝纤维化作用机制。方法分离大鼠肝星状细胞(HSC),于无包被塑料培养皿中原代培养7天,继以10-6mmol/L SA-B孵育,再加10ng/ml的转化生长因子β1(TGF-β1)或血小板衍生生长因子-BB(PDGF-BB)刺激。以Western blot法观察SA-B对TGF-β1或PDGF-BB刺激的HSC内ERK蛋白及其磷酸化表达的影响及对TGF-β1或PDGF-BB刺激的HSC表面TGF-β1Ⅰ型受体(TβRⅠ)、Ⅱ型受体(TβRⅡ)或PDGF受体β(PDGFR-β)表达的影响。结果SA-B可抑制原代正常培养9天的HSC及TGF-β1刺激的HSC中ERK1/2的磷酸化;对正常培养的HSC和TGF-β1刺激的HSC表面TβRⅠ和TβRⅡ的表达无明显影响。SA-B抑制原代正常培养9天的HSC和经PDGF-BB刺激的HSC中PDGFR-β的表达,但对PDGF-BB刺激的HSC中ERK1/2磷酸化没有明显作用。结论SA-B抑制TGF-β1诱导的HSC内ERK信号传导通路。这一抑制作用与HSC上TβR的表达无关,也与PDGF-BB在HSC内的ERK信号传导通路无关。SA-B对PDGF-BB在HSC内的信号传导通路的抑制作用在于抑制了HSC上PDGF受体的表达。 |
| 英文摘要: |
| ObjectiveTo explore the anti-hepatic fibrosis mechanisms of salvianolic acid B （SA-B）. MethodsHepatic stellate cells （HSCs） isolated from rats were primarily cultured in uncoated plastic culture dish for 7 days, then were incubated with 10 -6 mmol/L SA-B and stimulated with 10 ng/ml transforming growth factor-β1 （TGF-β1） or platelet-derived growth factor-BB （PDGF-BB）. Expressions of extracellular-regulated kinase（ERK） and its phosphorylation in HSC,and expressions of TGF β1 receptorⅠ （TβRⅠ） and Ⅱ（TβRⅡ） and PDGF receptor β （PDGFR-β） on the surface of HSC induced by TGF-β1 or PDGF-BB were detected with Western blot assay. ResultsSA-B inhibited the phosphorylation of ERK1/2 in HSC primary normally cultivated for 9 days stimulated or un-stimulated by TGF-β1, but could not affect the expressions of TβRⅠand TβRⅡ on the HSC surface; it down-regulated the expression of PDGFR-β, but had no obvious effect on the phosphorylation of ERK1/2 in those HSC stimulated or un-stimulated by PDGF-BB. ConclusionSA-B inhibits the ERK signal transduction induced by TGF-β1 in HSC, which is independent of the expressions of TβR on HSC surface and also free from the ERK signal transduction stimulated by PDGF-BB. And its inhibition on PDGF-BB signal transduction in HSC is by way of restraining the expression of PDGFR in HSC. |
| 关闭 |
扫描微信二维码，获取更多信息