论文部分内容阅读
为探讨转化生长因子-β1及组蛋白去乙酰化酶Sirt1和Sirt2在高血压诱导的血管平滑肌细胞缝隙连接蛋白-43表达及细胞增殖中的作用,研究了腹主动脉窄缩诱导高血压大鼠和正常大鼠胸主动脉转化生长因子-β1、缝隙连接蛋白-43、Sirt1和Sirt2,以及细胞增殖标志蛋白增殖细胞核抗原表达的变化;观察Sirt1和Sirt2在转化生长因子-β1刺激大鼠VSMCs缝隙连接蛋白-43的表达及细胞增殖中的作用。结果显示,高血压大鼠胸主动脉的转化生长因子-β1、缝隙连接蛋白-43、TGF-β1、Sirt1和Sirt2的表达及细胞增殖较正常大鼠均明显升高;转化生长因子-β1促进了大鼠血管平滑肌细胞缝隙连接蛋白-43的表达和增殖,Sirt1与Sirt2的抑制剂Salermide有效抑制了转化生长因子-β1诱导的血管平滑肌细胞缝隙连接蛋白-43的表达与细胞增殖。结果表明,高血压通过上调转化生长因子-β1来诱导VSMCs缝隙连接蛋白-43的表达和细胞增殖,而Sirt1和Sirt2可能在其中起调控作用。
To investigate the role of TGF-β1 and histone deacetylases Sirt1 and Sirt2 in hypertension-induced gap junction protein-4 expression and cell proliferation induced by vascular smooth muscle cells, we studied the effects of abdominal aortic constriction-induced hypertensive rats And the expression of TGF-β1, connexin-43, Sirt1 and Sirt2 in rat thoracic aorta and the expression of proliferating cell nuclear antigen (PCNA) in normal rat thoracic aorta. The effects of Sirt1 and Sirt2 on the expression of TGF-β1 in VSMCs The role of connexin-43 expression and cell proliferation. The results showed that the expression of TGF-β1, connexin-43, TGF-β1, Sirt1 and Sirt2 in thoracic aorta and the cell proliferation in hypertensive rats were significantly higher than those in normal rats. The expression of TGF-β1 The expression and proliferation of connexin-43 in rat vascular smooth muscle cells were significantly inhibited. Sirt1 and Sirt2 inhibitor Salermide effectively inhibited the expression of connexin-43 and the proliferation of vascular smooth muscle cells induced by TGF-β1. The results show that hypertension can up-regulate the expression of TGF-β1 and induce the expression of connexin-43 in VSMCs, while Sirt1 and Sirt2 may play a regulatory role.