摘要
目的探讨p38丝裂原活化蛋白激酶(p38MAPK)信号转导通路在转化生长因子β1(TGF-β1)诱导的肾小球系膜细胞(MC)分泌纤维连接蛋白(FN)过程中的作用。方法应用WesternBlot法检测系膜细胞内p38MAPK活性;应用ELISA法检测培养上清中FN。结果TGF-β1可诱导MC内p38MAPK活化,刺激15minp38MAPK活性增加,30min后,p38MAPK活性达高峰,1h后几乎恢复至正常水平,2h后再次升高,24h时仍高于正常。TGF-β1可促进MC分泌FN,p38MAPK特异性抑制剂SB203580显著抑制TGF-β1诱导的MC分泌FN。结论p38MAPK通路在TGF-β1引起的系膜细胞外基质成分之一的FN分泌增加中发挥一定的作用。SB203580能部分抑制TGF-β1诱导的FN的合成,可能对糖尿病肾病具有一定的治疗作用。
Objective： To investigate the role of p38 mitogen-activated protein kinase （MAPK） signal transduction pathway in regula- ting the fibronectin （FN） synthesis induced by transforming growth factor-β1 （TGF-β1） in rat mesangial cells （MC）. Methods： Western Blot analysis was used to detect the activity of p38 MAPK. FN was determined by enzyme-linked immunosorbent assay. Resuits： TGF-β1 activated p38 MAPK in MC, and the activity of p38 MAPK increased within 15 minutes after the administration of TGF-β1, reached the peak 30 minutes later, and returned to the baseline level 1 hour later. TGF-β1 up-regulated FN synthesis, and SB203580, the specific inhibitor of p38 MAPK, significantly down-regulated FN synthesis. Conclusion： P38 MAPK signal pathway may play an important role in regulating FN synthesis induced by TGF-β1 in MC.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2006年第3期246-248,共3页
Journal of China Medical University
基金
辽宁省教育厅高等学校科研基金资助项目(202013140)
