文章摘要
芮国华,潘荣华,姚〓刚,武晓春,徐玲玲.丹酚酸B对TGF-β1诱导的人肾小管细胞转分化的影响[J].南京医科大学学报,2009,29(12):1685~1689
丹酚酸B对TGF-β1诱导的人肾小管细胞转分化的影响
Prevent effects of salvianolic acid B on TGF-β1-induced epithelial mesenchymal transition in HK2 cells
投稿时间:2009-05-19  
DOI:10.7655
中文关键词: 丹酚酸B  转化生长因子-β1  上皮细胞-间充质细胞转分化
英文关键词: salvianolic acid-B  thansforming growth factor-β1  epithelialto-mesenchymal transition
基金项目:江苏省高校自然科学基础研究项目(08KJB320006);江苏省常州市社会发展项目(CS2006217)
作者单位
芮国华 溧阳市中医院肾内科,江苏 溧阳〓213300 
潘荣华 溧阳市中医院肾内科,江苏 溧阳〓213300 
姚〓刚 南京医科大学第二附属医院肾内科,江苏 南京〓210011 
武晓春 南京医科大学第二附属医院肾内科,江苏 南京〓210011 
徐玲玲 南京医科大学第二附属医院肾内科,江苏 南京〓210011 
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中文摘要:
      目的:探讨丹酚酸B对转化生长因子(TGF)-β1诱导的肾小管上皮细胞—间充质细胞转分化的影响?方法:将体外培养的人近端肾小管上皮细胞系(HK-2)细胞分为3组:①对照组:未加入丹酚酸B或者TGF-β1;②TGF-β1组:在细胞培养基中加入TGF-β1(浓度为5 ng/ml);③丹酚酸B+TGF-β1组:在细胞培养基中分别加入丹酚酸B和TGF-β1(浓度为5 ng/ml),按丹酚酸B的浓度分为A?B?C?D 4个亚组:丹酚酸B的浓度分别为A组:0.1 μmol/L,B组:1 μmol/L,C组:10 μmol/L,D组:100 μmol/L?72 h后,采用倒置相差显微镜观察细胞形态学变化;采用逆转录聚合酶链反应(RT-PCR)和免疫细胞化学染色检测细胞α-平滑肌肌动蛋白(α-SMA)和E-cadherin的表达情况?结果:TGF-β1组HK-2细胞从原有典型的上皮细胞形态转变为长梭形肌成纤维细胞形态;胞浆内大量表达α-SMA,同时E-cadherind的表达明显减少;不同剂量丹酚酸B治疗可减轻TGF-β1诱导的细胞形态学改变和胞浆内α-SMA的表达,同时E-cadherind的表达得到明显恢复,且呈剂量依赖性?结论:丹酚酸B具有阻止慢性肾脏疾病进行性发展的潜能,而这一作用与其能有效阻止TGF-β1诱导的HK-2细胞转分化有关?
英文摘要:
      Objective:To investigate the protective effects of salvianolic acid-B (Sal B) on the trans-differentiation of renal tubular epithelial cells and to elucidate the mechanism of Sal B on renal fibrosis. Methods:Human kidney proximal tubular cell line (HK-2) was used as the proximal tubular cell model. Cells were divided into six groups as follows:control group,transforming growth factor-β1 (TGF-β1) (5 ng/ml) group,TGF-β1 (5 ng/ml) plus Sal B (0.1 μmol/L,1 μmol/L,10 μmol/L,and 100 μmol/L) groups. Epithelialto-mesenchymal transition(EMT) was induced with 5 ng/mL of human TGF-β1. The effect of Sal B on cell morphology was observed by phase contrast microscopy,and the expressions of α-smooth muscle actin(α-SMA) and E-cadherin were measured by immunocytochemistry and RT-PCR. Results:Our results revealed that Sal B not only prevented the expression of α-SMA but also prohibited the decrease of the epithelial marker E-cadherin in HK-2 cells in a dose-dependent manner. Simultaneous incubation of Sal B with TGF-β1 could protect the change to the myofibroblast phenotype and restored the epithelial morphology of the HK-2 cells. Conclusion:These observations strongly suggest that Sal B is a potent inhibitor of TGF-β1-induced EMT and may be a promising agent for treating tubulointerstitial fibrosis.
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