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目的探讨p38丝裂素活化蛋白激酶(MAPK)信号通路在单核细胞趋化蛋白1(MCP-1)介导大鼠系膜细胞(MCs)增殖及纤连蛋白(FN)和Ⅰ型胶原(ColⅠ)表达中的调控作用。方法用四甲基偶氮唑盐比色法(MTT法)评估不同浓度的MCP-1(12.5、25、50、100ng/ml)及p38MAPK阻断剂SB203580(1、5、10μmol/L)于不同时间对体外培养的大鼠MCs的增殖作用。采用逆转录多聚酶链反应(RT-PCR)检测细胞内FN、ColⅠmRNA的表达。用ELISA法检测上清液FN、ColⅠ蛋白含量。结果MCP-1能刺激MCs的增殖,呈剂量和时间依赖性(P<0.05),而p38MAPK阻断剂明显抑制上述MCP-1的作用(P<0.01)。MCP-1能使细胞FN、ColⅠ的表达上调,而p38MAPK阻断剂能抑制其上调表达的作用。结论p38MAPK信号转导通路在MCP-1介导大鼠MCs增殖及FN和ColⅠ表达中起调控作用。MCP-1在系膜增生性肾小球肾炎(MsPGN)的发病中起一定的作用。
Objective To investigate the effects of p38 mitogen - activated protein kinase (MAPK) signaling pathway on the proliferation of rat mesangial cells (MCs) induced by monocyte chemoattractant protein 1 (MCP - 1) and the effects of fibronectin (FN) Col Ⅰ) expression in the regulation. Methods Different concentrations of MCP-1 (12.5, 25, 50, 100ng / ml) and p38MAPK blocker SB203580 (1,5,10μmol / L) were evaluated by MTT colorimetry Proliferation of rat MCs cultured in vitro at different times. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expression of FN and ColⅠmRNA. The contents of FN and Col I in the supernatant were detected by ELISA. Results MCP-1 stimulated the proliferation of MCs in a dose-and time-dependent manner (P <0.05), while p38 MAPK inhibitor significantly inhibited the effects of MCP-1 (P <0.01). MCP-1 can up-regulate the expression of FN and ColⅠ, while p38MAPK blockade up-regulated the expression of FN and ColⅠ. Conclusion p38MAPK signal transduction pathway plays a regulatory role in MCP-1-mediated MCS proliferation and FN and ColⅠ expression. MCP-1 plays a role in the pathogenesis of mesangial proliferative glomerulonephritis (MsPGN).