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N-acetylcysteine protects H9c2 cells against injuries induced by methyl-glyoxal / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 398-404, 2016.
Article Dans Chinois | WPRIM | ID: wpr-490679
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.

Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) langue: Chinois Texte intégral: Chinese Journal of Pathophysiology Année: 2016 Type: Article

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Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) langue: Chinois Texte intégral: Chinese Journal of Pathophysiology Année: 2016 Type: Article