Effect of pioglitazone on hypoxia/reoxygenation injury and protein kinase C expression in neonatal rat cardiomyocytes.
- Author:
Qi-wei ZHU
1
;
Hao WANG
;
Jin-yao ZHANG
;
Ping YE
;
Lei-ming LUO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Apoptosis; drug effects; Cell Hypoxia; physiology; Female; Ischemic Preconditioning, Myocardial; methods; Male; Myocardial Reperfusion Injury; physiopathology; prevention & control; Myocytes, Cardiac; enzymology; pathology; PPAR gamma; metabolism; Potassium Channels; metabolism; Primary Cell Culture; Protein Kinase C; genetics; metabolism; Rats; Rats, Sprague-Dawley; Thiazolidinediones; pharmacology
- From: Journal of Southern Medical University 2011;31(11):1819-1823
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of pioglitazone on hypoxia/reoxygenation injury and the expression of protein kinase C (PKC) in neonatal rat cardiomyocytes.
METHODSNeonatal Sprague-Dawley rat cardiomyocytes in primary culture were treated with pioglitazone or GW9662 for 24 h prior to hypoxia/reoxygenation injury. Cardiomyocyte apoptosis was evaluated with Hoechst33258 staining and the expression of PKC was detected using Western blotting.
RESULTSIn the early stage of hypoxia/reoxygenation injury, the apoptosis rates of the cardiomyocytes increased significantly from (0.20∓0.03)% of the control level to (12.22∓1.45)% (P<0.05). Pretreatment with pioglitazone significantly lowered the apoptosis rate of the cardiomyocytes with hypoxia/reoxygenation injury to (8.32∓0.89)%, and this effect was antagonized by GW9662, a specific blocker of peroxisome proliferators activated receptors γ (PPARγ). Pioglitazone did not cause increased expression of PKC in the cardiomyocytes.
CONCLUSIONPioglitazone can ameliorate neonatal rat cardiomyocyte injury induced by hypoxia/reoxygenation partially by activating PPARγ and does not increase the expression of PKC in the cells.
