Anti-apoptotic role of mitochondrial aldehyde dehydrogenase 2 in myocardial ischemia/reperfusion injury in diabetic rats.
- Author:
Hong-Ju WANG
1
;
Pin-Fang KANG
;
Hong-Wei YE
;
Ying YU
;
Xiao-Mei WANG
;
Qin GAO
Author Information
- Publication Type:Journal Article
- MeSH: Aldehyde Dehydrogenase; metabolism; Aldehyde Dehydrogenase, Mitochondrial; Animals; Apoptosis; drug effects; Caspase 3; metabolism; Diabetes Mellitus, Experimental; complications; enzymology; Ethanol; pharmacology; Male; Mitochondrial Proteins; agonists; metabolism; Myocardial Ischemia; enzymology; etiology; Myocardial Reperfusion Injury; enzymology; pathology; prevention & control; Myocardium; enzymology; pathology; Proto-Oncogene Proteins c-bcl-2; metabolism; Rats; Rats, Sprague-Dawley; bcl-2-Associated X Protein; metabolism
- From: Journal of Southern Medical University 2012;32(3):345-348
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the anti-apoptotic effect of aldehyde dehydrogenase 2 (ALDH2) on myocardial ischemia/reperfusion (I/R) injury in diabetic rats.
METHODSNormal male SD rats were divided into normal, diabetes and ethanol (the agonist of ALDH2) + diabetes groups. In the latter two groups, diabetes was induced by an intraperitoneal injection of 55 mg/kg STZ. Four weeks after the modeling, myocardial I/R was mimicked ex vivo, and lactate dehydrogenase (LDH) content in the coronary flow was determined. The activities of caspase-3 and ALDH2 were evaluated, and the expressions of Bcl-2 and Bax mRNA in the left anterior myocardium were detected using RT-PCR.
RESULTSIn diabetic group, LDH release and caspase-3 activity were increased, while ALDH2 activity and Bcl-2/Bax mRNA expression were decreased as compared to those in normal control group. Compared with the diabetic group, ALDH2 agonist ethanol significantly reduced LDH release and caspase-3 activity, increased ALDH2 activity and Bcl-2/Bax mRNA expression.
CONCLUSIONIn diabetic rats, enhanced ALDH2 expression can offer mycardial protection possibly in relation to suppress cell apoptosis.
