目的研究ERK1/2通路在血小板源性生长因子(PDGF)-CC诱导的鼠心肌纤维化中的作用及其可能的机制。方法取SD大鼠乳鼠心脏组织,差速贴壁法分离并纯化心肌成纤维细胞。按不同药物处理随机分成对照组(CON组)、PDGF-CC(P组)、PDGF-CC+ERK1/2抑制剂U0126(PU组)。MTT法检测心肌成纤维细胞的增殖,qRT-PCR法检测mRNA含量,Western blot法分析蛋白表达量。结果MTT法显示P组细胞数较CON组显著增加(P<0.01),而PU组细胞数较P组明显减少(P<0.01)。qRT-PCR法显示P组中PDGF-α受体(PDGFR-α)、ERK1、ERK2、Ⅰ型和Ⅲ型胶原蛋白(ColⅠ、ColⅢ)的mRNA表达水平均明显高于CON组(P<0.001),PDGFR-β的mRNA表达量在P组与CON组间差异无统计学意义。与P组相比,PU组中PDGFR-α、ERK1、ERK2、ColⅠ和ColⅢmRNA表达均明显下降(P<0.01)。Western blot法显示P组中磷酸化PDGFR-α(pPDGFR-α)、ERK1/2、p-ERK1/2、ColⅠ和ColⅢ的表达量均明显高于CON组(P<0.001),PU组中p-PDGFR-α、ERK1/2、p-ERK1/2、ColⅠ和ColⅢ蛋白表达量均显著低于P组(P<0.001)。结论 PDGF-CC可能通过结合PDGFR-α激活ERK1/2信号通路,诱导鼠心肌成纤维细胞过量增殖伴胶原蛋白的合成,参与心肌纤维化的发生。 Objective To investigate the role of ERK1 / 2 pathway in rat cardiac fibrosis induced by platelet-derived growth factor (PDGF) -CC and its possible mechanism. Methods The heart tissues of SD rats were isolated and purified by differential adherent method. The rats were randomly divided into control group (CON group), PDGF-CC group (P group) and PDGF-CC + ERK1 / 2 inhibitor U0126 group (PU group). The proliferation of cardiac fibroblasts was detected by MTT assay, the mRNA content was detected by qRT-PCR and the protein expression was analyzed by Western blot. Results MTT assay showed that the number of cells in P group was significantly increased compared with CON group (P <0.01), while the number of cells in PU group was significantly decreased compared with P group (P <0.01). qRT-PCR showed that mRNA expression levels of PDGF-αreceptors (PDGFR-α), ERK1, ERK2, typeⅠand typeⅢcollagen (ColⅠ, ColⅢ) in group P were significantly higher than those in group CON (P <0.001) The mRNA expression of PDGFR-β had no significant difference between P group and CON group. Compared with P group, the expression of PDGFR-α, ERK1, ERK2, ColⅠ and Col Ⅲ mRNA in PU group were significantly decreased (P <0.01). Western blot showed that the expression of phosphorylated PDGFR-α (pPDGFR-α), ERK1 / 2, p-ERK1 / 2, ColⅠand ColⅢ in group P were significantly higher than that in CON group The expressions of PDGFR-α, ERK1 / 2, p-ERK1 / 2, ColⅠ and Col Ⅲ were significantly lower than those in group P (P <0.001). Conclusion PDGF-CC may induce cardiac fibroblasts over-proliferation and collagen synthesis by binding to ERK1 / 2 signaling pathway and participate in the occurrence of myocardial fibrosis.