作　　者： ; ; ; ; ;

机构地区： 右江民族医学院附属医院

出　　处： 《中国动脉硬化杂志》 2013年第7期605-608,共4页

摘　　要： 目的探讨瑞舒伐他汀对转化生长因子β1(TGF-β1)诱导的新生大鼠心脏成纤维细胞增殖及其胶原合成与分泌的作用和可能机制。方法分离、培养新生SD大鼠的心脏成纤维细胞,采用CCK-8比色法测定细胞数目。用RT-PCR检测Ⅰ型胶原蛋白和Ⅲ型胶原蛋白mRNA的表达,用ELISA测定Ⅰ型胶原蛋白和Ⅲ型胶原蛋白含量,用Western blot检测心脏成纤维细胞Akt的蛋白表达。结果 CCK-8比色法显示,瑞舒伐他汀能抑制TGF-β1引起的心脏成纤维细胞增殖;RT-PCR结果显示,瑞舒伐他汀能抑制TGF-β1诱导的Ⅰ型胶原蛋白和Ⅲ型胶原蛋白mRNA的表达;ELISA结果显示,瑞舒伐他汀能抑制TGF-β1诱导的Ⅰ型胶原蛋白和Ⅲ型胶原蛋白分泌;Westernblot结果显示,瑞舒伐他汀能抑制TGF-β1诱导的Akt蛋白表达。结论瑞舒伐他汀可能通过抑制TGF-β1诱导的新生大鼠心脏成纤维细胞增殖、Ⅰ型和Ⅲ型胶原蛋白的合成与分泌来抑制TGF-β1诱导的心脏纤维化,其分子机制可能与抑制Akt信号通路有关。 Aim To investigate the effects and mechanism of rosuvastatin on TGF-β1-induced proliferation and collagen synthesis in neonatal rat cardiac fibroblasts. Methods Cardiac fibroblasts of neonatal SD rats were isolated and cultured, effect of rosuvastatin on fibroblast proliferation was detected by CCK-8, collagen synthesis was measured with real time-PCR, collagen secretion was checked by ELISA, Akt protein expression was tested by Western blot. Results Rosuvastatin dose-dependently inhibited TGF-β1-induced cardiac fibroblast proliferation, collagen synthesis and collagen secretion, and rosuvastatin could also inhibit Akt activity. Conclusions Rosuvastatin may inhibit TGF-β1-induced cardiac fibrosis through inhibiting cardiac fibroblast proliferation, collagen synthesis and collagen secretion. Its molecular basis may be associated with inhibiting Akt signaling pathway.

关 键 词： 心脏成纤维细胞 瑞舒伐他汀 细胞增殖 胶原蛋白 心脏纤维化

领　　域： [生物学]