Effects Of GPER On Cardiocyte After Hypoxia-reperfusion And Its Mechanism

Introduction:Several studies have recently demonstrated that G protein coupled receptor30(GPER) can directly bind to estrogen and mediate its action. Aims:Our aim is to investigate the effects of GPER on cardiocyte after myocardial hypoxia reperfusion injury in H9C2cell and its mechanism. We treated H9C2cell with a specific GPER agonist (G1),17β-estradiol(E2), or vehicle.Cells were subjected to20minutes of myocardial hypoxia followed by120minutes of reperfusion. They then were randomly assigned to three experimental groups:control, G1,E2. Bax and bcl-2levels were measured,hochest33258for cell apoptosis were performed,SOD,TNF-a and ATP were determined. To test the specificity of G1, we treated GPER-knockout cells with Gl,then tested above items. To study what is the relation between the effects of GPER and thioredoxin(Trx),we treated Trx-knockout cells with G1.We randomly assigned them to five experimental groups:control, empty vector,Gl, Trx-KO, Trx-KO+Gl,then tested above items.Results:Compared with vehicle-treated groups, G1and E2-treated groups had evaluated bcl-2level, decreased bax level and cell apoptosis， significantly increased SOD and ATP levels,decreased TNF-a level after ischemia-reperfusion. However, no obvious effects of G1was found in GPER-knockout or Trx-knockout cells.Conclusions:These results suggest that GPER activation provides a cardioprotective effect after hypoxia-reperfusion by inhibiting cardiocyte apoptosis.The effect is relevant to Trx.