摘要
目的观察苦参碱(Ma)对脂多糖(LPS)诱导的肾小球系膜细胞(MC)中信号转导子与转录激活子(STAT)分子1、3,结缔组织生长因子(CTGF)及血小板源性生长因子(PDGF)表达的影响,探讨苦参碱抑制增殖的机制。方法原代培养人胚肾小球系膜细胞并鉴定。实验分为正常对照组、脂多糖(10μg/ml)组、脂多糖(10μg/ml)+苦参碱(320μg/ml)组,分别于12、24、48h采用Real-TimePCR检测STAT1、3、CTGF及PDGF mRNA表达及Western blot检测p-STAT1、3蛋白表达。结果与正常对照组相比,在12、24、48h时间段,10μg/ml的LPS能够促进人肾小球系膜细胞增殖,320μg/ml的Ma对MC均有抑制增殖作用(P<0.01);在12、24、48h,LPS组STAT1、3、CTGF及PDGF mRNA增高,苦参碱处理组较LPS组表达明显降低,且在24、48h抑制明显(P<0.01);LPS组P-STAT1在12、24、48h蛋白表达均上调,p-STAT3在24、48h蛋白表达明显上调(P<0.01),与LPS组相比,苦参碱处理组p-STAT1、3蛋白表达均下调,但p-STAT3在12h表达下调不明显(P>0.05)。结论苦参碱抑制增殖的机制有可能是通过下调STAT1、3,降低CTGF及PDGF的分泌未实现的。
Objectives To determine the effects of Matrine（Ma） on signal transducers and activators of transcription（STAT） 1,3,connective tissue growth factor（CTGF） and platelet-derived growth factor（PDGF） in glomerular mesangial cells（MC） induced by lipopolysaccharide（LPS）,and to explore the protective mechanisms of Ma.Methods Ma were added to cultured glomerular mesangial cells which were exposed to LPS for 12,24 and 48 hours.Real time polymerase chain reaction were used to determine STAT1,3,CTGF,PDGF mRNA.The protein expression of STAT1,3 and p-STAT1,3 were observed by Western blot.Results Compared with the control group,MC proliferation of the LPS group（10μg/ml） significantly increased,which were suppressed in the Ma（320 μg/ml） group（P0.01） at 12、24、48 hours.The expression of STAT1,3,CTGF,PDGF mRNA and the levels of p-STAT1,p-STAT3 protein was significantly increased in MC under LPS medium at 12、24、48 hours,which were obviously lower in Ma group than those of the LPS group,especially at 24、48 hours.Conclusions The protective mechanisms of Matrine is considered to down-regulate the expression of STAT1,3,CTGF and PDGF.
出处
《临床儿科杂志》
CAS
CSCD
北大核心
2010年第2期178-182,共5页
Journal of Clinical Pediatrics
基金
甘肃省中青年自然科学基金项目(NoYS-011-A23-022)
甘肃省中医药科研项目(NoGZK-2008-5)
关键词
信号转导子与转录激活子
系膜细胞
脂多糖
苦参碱
结缔组织生长因子
血小板源性生长因子
signal transducers and activators of transcription
mesangial cells
lipopolysaccharide
Matrine
connective tissue growth factor
platelet-derived growth factor
