AIM:To investigate the protective effect of N-acetylcysteine (NAC) on H9c2 cells from injuries induced by methylglyoxal (MG) and the potential mechanism.METHODS:H9c2 cells were divided into control group, MG treatment group, NAC +MG treatment group, SP600125 pretreatment +MG group, NAC group and SP600125 group.The viability of the H9c2 cells was measured by CCK-8 assay.The protein levels of p-JNK and t-JNK were tested by Western blot .The changes of intracellular reactive oxygen species ( ROS) were evaluated by 2′, 7′-dichlorofluorescein di-acetate (DCFH-DA) staining.Mitochondrial membrane potential (MMP) was measured by rhodamine 123 (Rh123) stai-ning.The morphological changes in apoptotic cardiomyocytes were detected by Hoechst 33258 staining.RESULTS: Du-ring 100~800 μmol/L concentration range , MG caused significantly reduced viability of the H 9c2 cells in a dose-depend-ent manner.NAC had a protective effect on H9c2 cells against the injuries induced by MG during 500~1 500μmol/L con-centration range through raising cell viability , inhibiting cellular oxidative stress and improving MMP ( P <0.01 ) . SP600125,an inhibitor of JNK, showed the protective effect similar to NAC on H9c2 cells against MG-induced injuries, in-cluding attenuating oxidative stress , improving MMP and suppressing apoptosis .CONCLUSION: N-acetylcysteine offers obvious protective effect on H9c2 cells against the injuries induced by methylglyoxal .The underlying mechanisms may be associated with decreasing the production of ROS , ameliorating MMP , inhibiting the activation of JNK and suppressing ap-optosis.

AIM: To explore the roles of heat shock protein 90 (HSP90) in the blockage of hydrogen sulfide (H2S) against chemical hypoxia-mimetic agent (cobalt chloride, CoCl_2)-induced oxidative stress injuries in H9c2 cardiac cell. METHODS: H9c2 cells were treated with CoCl_2 to set up the chemical hypoxia-induced the model of cardiomyocyte injury. Sodium hydrosulfide (NaHS, a H2S donor) was added into medium for 30 min before CoCl_2 treatment. ATP content was detected by high performance liquid chromatogram (HPLC). Mitochondrial membrane potential (MMP) was measured by rhodamine123 (Rh123) staining and photofluorography. The activity of superoxide dismutase (SOD) was observed using a SOD kit. The expression of heme oxygenase-1 (HO-1) was evaluated by Western blotting. RESULTS: CoCl_2 at concentration of 600 μmol/L significantly reduced SOD activity, ATP level and MMP, and enhanced the expression of HO-1 in H9c2 cells. Pretreatment with 400 μmol/L NaHS dramatically inhibited the cytotoxicity induced by CoCl_2, increased SOD activity, ATP level and MMP, decreased HO-1 expression. 17-allylamino-17 demethoxygeldanamycine(17AAG), an inhibitor of HSP90, obviously blocked the inhibitory effect of H2S on the CoCl_2-induced cytotoxicity, reduced the levels of ATP and MMP, increased HO-1 expression. However, no significantly influence on SOD activity was observed. CONCLUSION: HSP90 may mediate the cardioprotection of H2S via inhibiting the oxidative stress induced by chemical hypoxia.