Protection of hypothermic preserved isolated rat hearts by resveratrol and its underlying mechanism.
- Author:
Wei-Ming SUN
;
Ming-Zhi ZHENG
;
Lei YING
;
Xiao-Ming YU
;
Si-Wen WU
;
Ying-Ying CHEN
;
Yue-Liang SHEN
;
Yang WANG
- Publication Type:Journal Article
- MeSH: Animals; Cryopreservation; Heart; drug effects; Male; Organ Preservation; Rats; Rats, Sprague-Dawley; Sirtuin 1; metabolism; Stilbenes; pharmacology
- From: Chinese Journal of Applied Physiology 2014;30(4):348-351
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate whether resveratrol (RES) plays a protective role in hypothermic preserved isolated rat hearts and whether it is mediated by regulation of silent information regulator protein-1 (Sirt-1) expression.
METHODSThe Langendorff model of isolated rat heart was used. After stored in different Celsior solution at 4 degrees C for 9 h, SD rat hearts were randomly divided into 7 groups: blank control group;9 h group (soley hypothermic preservation for 9 h); RES group (3, 10, 30 micromol/L RES treatment plus hypothermic preservation for 9 h ), niacinamide (NAM) group (40 micromol/L NAM added in Celsior solution plus hypothermic preservation for 9 h), RES + NAM group (30 micromol/L RES and 40 micromol/L NAM were added in Celsior solution plus hypothermic preservation for 9 h). The morphological changes of cardiomyocytes were detected by the HE staining with the light microscope. The mRNA and protein expression levels of Sirt-1 were detected by Real-Time PCR and Western blot respectively.
RESULTS(1) Compared with the blank control group, myocardiocytes were injured remarkably in the 9 h group and the Sirt-1 mRNA and protein expression levels were decreased significantly (P < 0.01); (2) Compared with the 9 h group, rat myocardial injury was alleviated gradually in 3, 10, 30 micromol/L RES group and the Sirt-1 mRNA and protein expression levels were increased in a dose-dependent manner (P < 0.05); (3) The above protective effects of RES were attenuated by Sirt-1 inhibitor NAM.
CONCLUSIONRES can protect myocardiocytes from injury caused by long range hypothermic preservation and this protective effect maybe mediated by upregulation of Sirt-1 expression.