尾加压素Ⅱ促进大鼠心肌胶原蛋白表达及乳鼠心肌成纤维细胞的增殖

摘要

Objective To investigate the effect of urotensin Ⅱ on myocardial fibrosis in rats.Methods The pressure overload animal model was established in rats by abdominal aorta coarctation.The rats were divided into sham operation group,modeled for 4,8 and 12 weeks group.The expression of U Ⅱ,GPR14,col-Ⅰ,col-Ⅲ,and PKA in cardiac tissues was detected by Western blot.Isolated and cultured cardiac myofibroblasts (CFs) from new-born SD rats were treated with U Ⅱ,KT5720 or SB-611812,and then the proliferation of CFs was observed by micro scope and CKK-8.Results The expression of U Ⅱ,GPR14,col-Ⅰ,col-Ⅲand PKA increased markedly in cardiac tissues of model rat,which were time-dependent.U Ⅱ promoted the proliferation of CFs (P＜0.05),which could be inhibited by KT5720 or SB-611812.Conclusions U Ⅱ/UT system promotes the occurring and development of myocardial fibrosis.%目的 探讨尾加压素Ⅱ(UⅡ)对大鼠心肌纤维化的影响.方法 腹主动脉缩窄术建立慢性压力超负荷大鼠心力衰竭模型,大鼠分为假手术组、造模4、8和12周组.利用Western blot分析心肌组织中UⅡ、G蛋白偶联受体(GPR14)、胶原Ⅰ(col-Ⅰ)、Ⅲ(col-Ⅲ)及蛋白激酶A(PKA)的表达.体外培养乳鼠成纤维细胞,分为对照组、UⅡ处理组、UⅡ+KT5720处理组及UⅡ+SB-611812组.镜下观察及CKK-8法检测细胞增殖.结果 模型组大鼠心肌组织中UⅡ、GPR14、eol-Ⅰ、col-Ⅲ蛋白及PKA的表达显著增加,且呈时间依赖性.UⅡ促进乳鼠成纤维细胞(CFs)的增殖(P＜0.05),而KT5720、SB-61 1812可抑制UⅡ对乳鼠成纤维细胞的促增殖作用.结论 UⅡ及其受体系统促进大鼠心肌纤维化的发生发展.