Activation of mitochondrial aldehyde dehydrogenase 2 and inhibition of mitochondrial permeability transition pore involved in cardioprotection of ethanol postconditioning.
- Author:
Zheng-hong LI
1
;
Cui-rong JIANG
;
Man-li XIA
;
Hong-wei YE
;
Su-dong GUAN
;
Qin GAO
Author Information
- Publication Type:Journal Article
- MeSH: Aldehyde Dehydrogenase; drug effects; genetics; metabolism; Aldehyde Dehydrogenase, Mitochondrial; Animals; Ethanol; pharmacology; In Vitro Techniques; Ischemic Postconditioning; L-Lactate Dehydrogenase; metabolism; Male; Mitochondria, Heart; drug effects; metabolism; Mitochondrial Membrane Transport Proteins; drug effects; metabolism; Mitochondrial Proteins; drug effects; genetics; metabolism; Myocardial Reperfusion Injury; metabolism; pathology; prevention & control; Myocardium; metabolism; pathology; RNA, Messenger; genetics; Rats; Rats, Sprague-Dawley
- From: Journal of Zhejiang University. Medical sciences 2010;39(6):566-571
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate whether activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2) and inhibition of mitochondrial permeability transition pore (mitoPTP) were involved in the cardioprotection of ethanol postconditioning in isolated rat heart.
METHODSHearts isolated from male Sprague-Dawley rats were perfused on a langendorff apparatus and subjected to 30 min of regional ischemia (occlusion of left anterior descending artery) followed by 120 min of reperfusion. The ventricular hemodynamic parameters and lactate dehydrogenase (LDH) release during reperfusion were measured. Infarct size was measured by TTC staining method and the expression of ALDH2 at mRNA level of left anterior myocardium was detected by RT-PCR.
RESULTIn contrast to ischemia and reperfusion, ethanol postconditioning improved the recovery of left ventricular developed pressure, maximal rise/fall rate of left ventricular pressure during reperfusion, reduced LDH release and infarct size. The expression of ALDH2 mRNA level was increased. Administration of mitoPTP activator atractyloside attenuated the effect of ethanol postconditioning, LDH release and infarct size were increased, and the recovery of hemodynamic parameters was inhibited. The expression of ALDH2 mRNA was decreased.
CONCLUSIONEthanol postconditioning has cardioprotection effect, which may be associated with upregulating mitochondrial ALDH2 mRNA expression and inhibiting the opening of mitochondrial permeability transition pore.
