Protective mechanism of salubrinal against apoptosis induced by lipopolysaccharide in H9C2 cardiomyocytes
10.3760/cma.j.issn.1673-4912.2012.05.018
- VernacularTitle:Salubrinal抑制脂多糖诱导H9C2心肌细胞凋亡的保护机制
- Author:
Jingmei DONG
;
Yali LIU
- Publication Type:Journal Article
- Keywords:
Lipopolysaccharide;
Endoplasmic reticulum stress;
Mitochondria;
Apoptosis;
Cardiomyocytes
- From:Chinese Pediatric Emergency Medicine
2012;19(5):507-509
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanism of apoptosis induced by endoplasmic reticulum stress during sepsis.Methods Septic model of H9C2 cells was established by lipopolysaccharide (LPS).CHOP mRNA,mitochondrial membrane potential (MMP) and apoptosis were assessed by real-time PCR,flow cytometry respectively at LPS administration 24 h with or without salubrinal (inhibitor of endoplasmic reticulum stress).Results The expression of CHOP mRNA and apoptosis were upregulated,but MMP was decreased after LPS exposure 24 h compared with control group[2.40 ±0.30 vs 1.00 ±0,(16.58 ±2.71) ％ vs (3.85 ± 1.07) ％,1.07 ± 0.33 vs 2.62 ± 0.51,P ＜ 0.05).Compared with LPS group,salburinal pretreatment decreased LPS-induced upregulation of CHOP mRNA (1.60 ± 0.23 vs 2.40 ± 0.30,P ＜ 0.05),meanwhile,salburianl alleviated MMP(1.85 ± 0.31 vs 1.07 ± 0.33,P ＜ 0.05) and LPS-induced apoptosis [(6.05 ± 1.48) ％ vs (16.58 ± 2.71) ％,P ＜ 0.05].Conclusion Salubrinal plays a cytoprotective role against apoptosis induced by LPS through inhibition of CHOP mRNA,which leads to mitochondrial impairment.Endoplasmic reticulum stress may induce apoptosis via mitochondrial pathway in the septic model of H9C2 cardiomyocytes.
