| Objective: To investigate the delayed protective effects of sodium ferulate(SF) on myocardial cells A/R injury after 24 hr administration of SF, and futher to clarify the protective role may be involved in ERK1/2-HSP70 by using ERK1/2 specific blocker PD184352 and plasmid pSilencer-shHSP70.Method: Cultured neonatal rat myocardial cells were randomly divided into six groups: Control group; anoxia reoxygenation (A/R) group; delayed preconditioning (DP) group; SF group; PD184352 group; HSP70-shRNA group. After the treatment, the cell viability and lactate dehydrogenase(LDH) were detected; the content of MDA and the activities of SOD, GPx and catalase activities were assayed, the expression of HSP70,SOD,GPx and Catalase in cytoplasm was detected by Western blotting.Results:①Pretreated with 3.36μM·L-1SF 24hr ago, the cellular survival was significantly increased(p<0.01), while the LDH activity and the content of MDA were markedly decreased(p<0.01), besides, total antioxidant status including SOD, GPx and catalase activities increased(p<0.01). The protective roles of SF were weakened or abolished after intervention of PD184352 and HSP70-shRNA.②Pretreated with 3.36μM·L-1SF 24hr ago, the expression of HSP70 was markedly increased(p<0.01), while expressions of SOD, GPx and catalase were significant change(p>0.05). The increased expression of HSP70 induced by SF was inhibited by PD184352 and HSP70-shRNA(p<0.01).Conclusion: SF could play a pharmacological delayed protection role. The protective mechanism of SF might be involved in increased expression of HSP70 by activating ERK1/2 signaling pathway.SF have not affected the expression of SOD, GPx and catalase, but induced increase of HSP70 as a molecular chaperone, could have stabilized and protected the structure of endogenous antioxidant enzymes to maintain its biological activity, thus enhancing the ability of myocardial cells against free radical damage. |
PDF Full Text Request