Protective effect of metformin on H9C2 rat myocardial cell damage induced by saturated fatty acid
10.3969/j.issn.1671-8348.2017.20.002
- VernacularTitle:二甲双胍对饱和脂肪酸诱导的大鼠H9C2型心肌细胞损伤的保护作用研究
- Author:
Xiao ZHANG
;
Hongming ZHANG
;
Danan LIU
;
Xiaoyan LI
- Keywords:
metformin;
NF-Kappa B;
chemokine;
adenosine activated protein kinase
- From:
Chongqing Medicine
2017;46(20):2741-2743
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanisms of metformin (Met) for protecting H9C2 myocardial cells damage induced by saturated fatty acids (palmitic acid,PA) in rats.Methods Rat H9C2 myocardial cell lines in blank control group,PA group and three different concentrations of metformin and PA combination groups were cultured for 24 h.Then Western blot was adopted to detect the protein expression of nuclear factor κB p65 (NFκB p65),intercellular cell adhesion molecule-1 (ICAM1),phosphorylated inhibitor of nuclear factor κB (p-IκBα) and phosphorylated adenosine monophosphate activated protein kinase(p-AMPK);the quantitative real-time PCR(qRT-PCR) was used to detect the mRNA expression of nuclear factor of nuclear factor κB(NFκB),chemokine (C-C motif) ligand 2 (CCL2) andintercellular cell adhesion molecule-1(ICAM1).Results Compared with the control groups,the protein expression of NFκB p65,p-IκBα and ICAM1 in the PA group was increased (P<0.05);compared with the PA group,the protein expression of NFκB p65,IκBα and ICAM1 in the Met+PA combination groups was decreased in various degrees with the Met concentration increase (all P<0.05),while the protein expression of p-AMPK was significantly risen with the Met concentration increase (all P<0.05).Compared with the control group,the mRNA expression of CCL2 and ICAM1 in the PA group was increased (P<0.05);compared with the PA group,the mRNA expression of CCL2 and ICAM1 in the Met+PA combination groups was decreased (P<0.05).Conclusion Met can alleviate H9C2 myocardial cellular damage caused by saturated fatty acid inducing increase of CCL2 and ICAM1 expression.
