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研究表明,心肌肌浆网钙泵(SERCA2)的异常在心力衰竭(心衰)的发展机制中发挥重要作用。很多因素可以调节SERCA2的活性,最主要的是受磷蛋白的调节。而受磷蛋白的磷酸化及去磷酸化分别由蛋白激酶A和磷酸酶1α调控。目前国内少见关于心衰蛋白激酶A和磷酸酶1α变化的报道。本实验通过用超容量负荷联合压力负荷制备家兔心衰模型,进而观察心衰时蛋白激酶A和磷酸酶1α的变化,从而探讨心衰的部分病理生理机制。
Studies have shown that the abnormality of cardiac sarcoplasmic reticulum calcium pump (SERCA2) plays an important role in the pathogenesis of heart failure (heart failure). Many factors can regulate the activity of SERCA2, the most important is regulated by phosphoproteins. Phosphorylation and dephosphorylation of phosphoproteins are regulated by protein kinase A and phosphatase 1α, respectively. Currently rare on the heart failure protein kinase A and phosphatase 1α changes reported. In this study, rabbit models of heart failure were prepared by overloading combined with stress load, and then the changes of protein kinase A and phosphatase 1α in heart failure were observed to explore some pathophysiological mechanisms of heart failure.