RGS14通过抑制TAK1改善急性心肌梗死的作用及机制研究OA

Objective This study aims to investigate the role and mechanism of regulator of G-protein signaling 14(RGS14)protein in acute myocardial infarction(AMI).Methods The RGS14 knockout mice were selected to construct AMI model.The cardiac tissue and serum of mice were collected 24 h after modeling,the degree of inflammatory infiltration in the cardiac tissue was analyzed by immunohistochemical analysis,and biochemical analyzer detects serum biochemical indicators.Overexpression and knockdown adenovirus were constructed in vitro and transfected into primary rat cardiomyocytes.RT-qPCR and Western blot were used to detect the expression of RGS14,inflammation and apoptosis related markers mRNA and protein.TUNEL staining was used to analyze the apoptosis of heart tissue.Results The expression of RGS14 in myocardial cells of AMI model mouse was downregulated.Compared with wild-type mice,RGS14 knockout mice exhibited increased AMI induced cardiac dysfunction,inflammatory response,and apoptosis.Conversely,overexpression of RGS14 inhibited cardiomyocyte apoptosis in vitro.The protective effect of RGS14 on AMI injury is closely related to its inhibition of TAK1-JNK/p38 signaling pathway activation.Inhibition of TAK1 alleviates the adverse effects of RGS14 knockdown on AMI in vitro.Conclusion RGS14 exerts a protective function in the process of inflammation and apoptosis after AMI,and alleviates cardiac dysfunction by inhibiting the activation of TAK1,which provides a new potential for the treatment of AMI.