缓激肽对PDGF诱导的肾小球系膜细胞增殖的影响

目的]探讨缓激肽（bradykinin,BK）对血小板源生长因子（PDGF）诱导的系膜细胞增殖的影响及与ERK信号途径相关性。方法]BK预孵系膜细胞,采用PDGF-BB刺激系膜细胞,应用MTT法测细胞增殖,ELISA法测Ⅳ型胶原,应用Western法检测ERK蛋白表达,并应用BK受体特异性阻断剂HOE-140进一步研究BK对ERK通路的作用。结果]（1）BK抑制PDGF所致的系膜细胞增殖,与单用PDGF-BB组比较差异有非常显著性意义（P〈0.05）。（2）BK抑制PDGF-BB所致系膜细胞Ⅳ型胶原分泌,与单用PDGF-BB组比较差异有显著性意义（P〈0.05）。（3）BK抑制PDGF-BB所致的系膜细胞ERK1/2磷酸化表达,与单用PDGF-BB组比较差异有显著性意义（P〈0.01）,HOE-140能阻断BK对于PDGF-BB/ERK1/2途径磷酸化的抑制作用。结论]BK抑制PDGF诱导的系膜细胞增殖及细胞外基质分泌,该作用可能是通过抑制PDGF诱导的ERK1/2途径激活实现。

Inhibition of bradykinin to PDGF-induced mesangial cells proliferation

Objective] To investigate the effects of bradykinin(BK) on platelet-derived growth factor(PDGF)-induced mesangial cells(MC) proliferation,collagen secretion and ERK signal pathway.Methods] MC was stimulated by BK with different concentrations as well as with PDGF-BB,or pretreated with HOE-140,a BK-B2 receptor special blocker.MTT method and ELISA assay were performed to detect the levels of proliferation and ColⅣ used for secretion after treatment.Western blotting was performed to observe the instant expression of ERK1/2 phosphorylation.Results](1) BK inhibited PDGF-induced mesangial cells proliferation.(2) BK inhibited PDGF-induced ColⅣsecretion.(3) BK downregulated PDGF-induced ERK1/2 phosphorylation and the inhibitory effects of BK on PDGF-BB was completely abolished by addition of HOE-140.Conclusion] BK could inhibit PDGF-induced proliferation and ColⅣ secretion in mesangial cells by inhibiting phosphorylation of ERK1/2.