关键词: 木犀草素, 氧化应激损伤, RISK信号通路

Abstract: In order to investigate whether luteolin can protect heart against myocardial oxidative stress injury via reperfusion injury salvage kinase (RISK) signaling pathway we use myocardial H9c2 cells were pretreated with luteolin at 1,50,100 and 150 μmol / L respectively,while cell oxidative stress injury was induced by adding 650 μmol / L H₂O₂.Cell viability was detected by MTT assay (MTT assay).Then,H9c2 cells were pretreated with luteolin at the optimal concentration and mitochondrial membrane potential was detected by laser confocal microscopy.Western blot was used to detect the level of P-ERK1 / 2,P-Akt,P-GSK-3β and apoptosis-related protein Cytochrome c.Finally we found that compared with the control group,cells pretreated with different concentrations of luteolin showed an increase in cell survival rate,which reached the pink at 100 μmol / L.Compared with H₂O₂ group,pretreatment with 100 μmol / L luteolin could significantly reduce the intensity of TMRE (tetramethylrhodamine ethyl ester) and prevent oxidative damage of cells induced by H₂O₂.At the same time,luteolin pretreatment could decrease the expression of Cytochrome C,but increase the expression of P-GSK-3β,P-Akt and P-ERK1 / 2,which were inhibited by wortmannin (PI3K inhibitor) and PD98059 (ERK1 / 2 inhibitor).So we think that Luteolin preconditioning reduces oxidative stress injury by decreasing GSK-3β activity via RISK signaling pathway and then inhibiting mPTP opening.

Key words: luteolin, oxidative stress injury, RISK signaling pathway