Effect of Akt1 gene transfection on mitochondrial permeability transition after myocardium ischemia-reperfusion in rat
- VernacularTitle:转染Akt1基因对缺血再灌注大鼠心肌线粒体通透性转换的影响
- Author:
Jing WANG
;
Dongye LI
;
Yong XIA
;
Yuanyuan LUO
;
Dan CHEN
;
Defeng PAN
;
Hong ZHU
;
Zhuoqi ZHANG
;
Tongda XU
- Publication Type:Journal Article
- Keywords:
Genes;
Akt1;
Reperfusion injury;
Mitochondrial permeability transition
- From:
Chinese Journal of Pathophysiology
2010;26(1):80-85
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effects of Akt1 gene transfection into myocardium after ischemia-reperfusion (I/R) on mitochondrial permeability transition. METHODS:Forty adult male SD rats were divided randomly into five groups with 8 rats each:control group,I/R group,Ad-gene group,Ad-blank group and Ad-inhibitor group. The rats in Ad-gene group were injected with 30 μL Lipofectamine 2000 solution including Akt1 gene to the myocardium 48 h before ischemia while those in control group and I/R group were injected with PBS of the same volume. Rats in Ad-blank group were injected with Lipofectamine 2000 of the same volume into myocardium. In Ad-inhibitor group 30 μL Lipofectamine 2000 and gene complexes with LY294002 were injected. Hemodynamics,apoptotic index,the concentrations of lactate dehydrogenase,creatine kinase,the expression of Akt1,cytosolic,mitochondrial cytochrome C and MPT were also measured. RESULTS:The lowest level of Akt1 protein expression was observed in control group. The protein expression of Akt1 in Ad-gene group was higher than that in I/R group,Ad-blank group and Ad-inhibitor group. The AI,LDH and CK in Ad-gene group were significantly lower than those in other groups except control group. Transfection of Akt1 markedly reduced the loss of mitochondrial cytochome C after I/R injury. Ad-gene transfection led to a significant increase in absorbance at 540 nm compared to I/R group,Ad - black group and Ad-inhibitor group (P<0.05). CONCLUSION:Akt1 gene prevents myocardial apoptosis after I/R injury. Akt1 gene also inhibits the opening of mitochondria permeability transition and protects mitochondrial functions of myocardium in I/R injury.
