Changes of expression and distribution of prohibitin in oxidative stressed cardiomyocyte and its biological significance.
- Author:
Zhe REN
1
;
Ling-jia QIAN
;
Zhi-hua YANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Cells, Cultured; L-Lactate Dehydrogenase; metabolism; Mitochondria, Heart; metabolism; Myocytes, Cardiac; metabolism; pathology; Oxidative Stress; Rats; Rats, Wistar; Repressor Proteins; metabolism
- From: Chinese Journal of Applied Physiology 2007;23(2):173-177
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo approach the expression of prohibitin in oxidative stressed cardiomyocytes.
METHODSThe oxidative stress model was established by treating neonatal cardiomyocytes with H2O2. Injury of cardiomyocytes were evaluated by detecting the LDH activity and MTT cell survival rate.The expression level of prohibitin was examined via the Western-blotting. The ability of mitochondrial oxidative phosphorylation was determined by measuring ATP synthesis via H+ -ATPase. Mitochondrial membrane potential was detected by flow cytometry using Rhl23.
RESULTSLDH activity increased significantly after exposure to H202, while the cell survival rate decreased by 34.51%-65.5%. The contents of mitochondrial prohibitin in stress group was much higher than that in control group. At the same time, the ability of ATP synthesis decreased by 60% and mitochondrial transmembrane potential decreased too.
CONCLUSIONExpress of prohibitin in oxidative stress cardiomyocytes was compensated increase. Prohibitin translocated to mitochondria after oxidative stress. Oxidative stress led to mitochondrial dysfunction.
