Effect of resveratrol on heart function of rats with adriamycin-induced heart failure.
- Author:
Gui-ying WANG
1
;
Yong-mei WANG
;
Li-nan ZHANG
;
Qian LI
;
Hua YUE
;
Cui-miao SONG
;
Jing-kun FENG
;
Na WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Doxorubicin; Heart; physiopathology; Heart Failure; chemically induced; pathology; physiopathology; Male; Malondialdehyde; blood; Myocardium; pathology; Nitric Oxide; blood; Nitric Oxide Synthase; blood; Random Allocation; Rats; Rats, Sprague-Dawley; Stilbenes; pharmacology; Superoxide Dismutase; blood
- From: China Journal of Chinese Materia Medica 2007;32(15):1563-1565
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the protective effects of resveratrol (RES) on the heart function of the rats with adriamycin-induced heart failure.
METHODThirty adult male SD rats were randomly divided into 5 groups: normal control (NC) group, adriamycin (ADR) group, RESL + ADR group, RES(H) + ADR group and RES group. RES of 30, 120, 120 mg x kg(-1) x d(-1) was given intraperitoneally (ip) once a day for 3 days in RES(L) + ADR group, RES(H) + ADR group and RES group respectively. The other two groups were given the same amount of normal saline the same way. On the 4h day,ADR of 10 mg x kg(-1) was given intraperitoneally once to induce myocardium injury model. After twenty-four hours, the pathological and biochemical changes of the myocardium were examined.
RESULTAs compared with NC group, the MDA, NO and NOS of the ADR group were significantly higher (P < 0.05), and the SOD of the ADR group were markedly lower (P < 0.05). As compared with ADR group, the indexes in RES(L) + ADR group, RES(H) + ADR group were exactly opposing, and took on dose dependance (P < 0.05). Light microscopic morphometry of the heart samples of the rats in ADR + RES(L, H) groups revealed typical diminishing of damage.
CONCLUSIONRES can relieve the toxic effects of ADR on myocardium, and the cardioprotective effects may be correlated with its antioxidant activity and downregulation of NO.