Role of autophagy in HL-1 cardiomyocyte injury induced by lipopolysaccharide
10.3760/cma.j.issn.0254-1416.2011.10.020
- VernacularTitle:自吞噬在脂多糖诱导HL-1心肌细胞损伤中的作用
- Author:
Jianjun XU
;
Le YANG
;
Jian LI
;
Aitao WANG
;
Xiaojing ZOU
;
Shanglong YAO
- Publication Type:Journal Article
- Keywords:
Autophagy;
Lipopolysaccharide;
Cardiomyocytes;
Mitochondria;
Apoptosis
- From:
Chinese Journal of Anesthesiology
2011;31(10):1235-1238
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the role of autophagy in HL-1 cardiomyocyte injury induced by lipopolysaccharide( LPS).Methods Primary cultured HL-1 cardiomyocytes were randomly divided into 4 groups ( n =15each): normal control group( group C),LPS group,rapamycin( a autophagy inducer) group( group R) and 3-MA(a autophagy inhibitor) group.In group C cardiomyocytes were cultured continuously for 24 h.In group LPS cardiomyocytes were incubated with LPS (final concentration 1 μg/ml) for 24 h.In groups R and 3-MA,rapamycin and 3-MA was given 48 h before LPS (final concentration 1 μg/ml) incubation with final concentration of 0.2 μg/ml and 10 mmol/L respectively.The lipidated microtubule-associated protein 1 light chain 3 Ⅱ (LC3 Ⅱ ) expression,mitochondrial membrane potential,autophagosome number and optical density of mitochondria were determined,and ultrastructure of mitochondria was observed at 4 h of LPS incubation.Apoptosis rate and Caspase-3 activity were determined at 24 h of LPS incubation.Results LPS significantly increased LC3 Ⅱ expression,autophagosome number,optical density of mitochondria,apoptosis rate and Caspase-3 activity,decreased mitochondrial membrane potential in group LPS as compared with group C ( P ＜ 0.05).The LC3 Ⅱ expression,autophagosome number and mitochondrial membrane potential were higher,optical density of mitochondria,apoptosis rate and Caspase-3 activity lower in group R than in group LPS( P ＜ 0.05).The LC3 Ⅱ expression,autophagosome number and mitochondrial membrane potential were lower,optical density of mitochondria,apoptosis rate and Caspase-3 activity higher in group 3-MA than in group LPS (P ＜ 0.05).Mitochondrial histopathologic injury was reduced in group R and aggravated in group 3-MA as compared with group LPS.Conclusion Autophagy can reduce LPS-induced HL-1 cardiomyocyte injury by improving mitochondrial function and inhibiting apoptosis.
