Abstract: ［Abstract］ Objective〖HTSS〗〓To study the protective mechanism of resveratrol(RES) on H9C2 cells injury induced by two cobalt chloride(CoCl2).
〖HTH〗〖WTHZ〗Methods〖HTSS〗〓CoCl2 （500 μmol/L） was used to treat H9C2 cardiac muscle cell for 24 h in order to establish H9C2 myocardial cell hypoxia injury model. The experiment was divided into five groups: blank control group(control); model injury group(H9C2 cells were pretreated with 0.1% DMSO culture medium for 24h, and then they were continued to treat by 500μmol/L CoCl2 for 24h); low dose RES group(H9C2 cells were pretreated with 12.5μmol/L RES for 24h, and then they were continued to treat by 500μmol/L CoCl2 for 24h); medium dose RES group(H9C2 cells were pretreated with 25μmol/L RES for 24h, and then they were continued to treat by 500μmol/L CoCl2 for 24h); high dose RES group(H9C2 cells were pretreated with 50μmol/L RES for 24h, and then they were continued to treat by 500μmol/L CoCl2 for 24h). MTT method was used to evaluate the viability of H9C2 myocardial cell. Morphological changes of H9C2 nucleus were observed by Hoeschst 33342 staining. The changes of mitochondrial membrane potential, intracellular reactive oxygen species(ROS) production and cell apoptosis were detected by flow cytometry in H9C2 cells. Western Blot was used to investigate the changes of apoptosis related proteins in H9C2 cells.
〖HTH〗〖WTHZ〗Results〖HTSS〗〓MTT results showed that RES concentration dependently inhibited the decrease of H9C2 cell viability induced by CoCl2. Hoeschst 33342 staining showed that RES concentration dependently inhibited the appearance of H9C2 cells apoptosis induced by CoCl2. Flow cytometry revealed that RES concentration dependently inhibited ROS production, decreased mitochondrial membrane potential, and increased apoptosis in H9C2 cells induced by CoCl2. Western blot showed that RES concentration dependently inhibited the increase of proapoptotic proteins(Bax, cleavedcaspase3, cleavedcaspase9) and decreased expression of apoptotic protein(Bcl2) in H9C2 cells induced by CoCl2.
〖HTH〗〖WTHZ〗Conclusion〖HTSS〗〓RES has the protective effect on H9C2 myocardial cell injury induced by CoCl2, the mechanism may be related with inhibiting the increase of ROS induced by CoCl2 and decreasing the mitochondrial membrane potential, thus hindering the occurrence of mitochondrial apoptosis in H9C2 cells.

Key words: myocytes, cardica, Resveratrol, apoptosis