N-acetylcysteine protects H9c2 cells against injuries induced by methyl-glyoxal
10.3969/j.issn.1000-4718.2016.03.003
- VernacularTitle:N-乙酰半胱氨酸对抗丙酮醛引起的心肌细胞损伤
- Author:
Xiaobian DONG
;
Juan WU
;
Xiaodong ZHUANG
;
Zena HUANG
;
Xun HU
;
Xinxue LIAO
- Publication Type:Journal Article
- Keywords:
H9c2 cells;
N-acetylcysteine;
Methylglyoxal;
c-Jun N-terminal kinase
- From:
Chinese Journal of Pathophysiology
2016;32(3):398-404
- CountryChina
- Language:Chinese
-
Abstract:
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.
