Effect of kinetin on ovary and uterus in D-galactose-induced female mouse model of aging.
- Author:
Jiang-Hong SUN
1
,
2
;
Yu-Mei LIU
;
Tong CAO
;
Wu-Qing OUYANG
Author Information
1. College of Veterinary Medicine, Northwest A&F University, Yangling 712100, China
2. College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471003, China. E-mail: oywq506@sina.com.
- Publication Type:Journal Article
- MeSH:
Aging;
Animals;
Estradiol;
metabolism;
Estrous Cycle;
drug effects;
Female;
Galactose;
Kinetin;
pharmacology;
Mice;
Organ Size;
Ovary;
drug effects;
Uterus;
drug effects
- From:
Acta Physiologica Sinica
2013;65(4):389-394
- CountryChina
- Language:Chinese
-
Abstract:
The present study was to investigate the effect of kinetin on ovary and uterus of D-galactose-induced female mouse model of aging. Aging female mice model caused by D-galactose were used as model group, the aging model mice intragastrically administered with kinetin solution (daily 25 mg/kg or 50 mg/kg) were used as kinetin groups, and the mice with solvent as normal group (n = 20). To detect the effects of kinetin, estrous cycle, estradiol content, ovarian and uterine wet weight and organ index, SOD and GSH-Px activities, MDA and total protein contents, as well as the reserve function of ovaries were examined. The results showed that, kinetin-induced changes in two kinetin groups were observed, compared with the model group: (1) the estrous cycle was shortened; (2) serum estradiol content was significantly increased; (3) the wet weights of the ovary and uterus were increased significantly; (4) SOD and GSH-Px activities of ovary and uterus were significantly higher; (5) the MDA contents of the ovary and uterus were reduced significantly; (6) total protein contents of the ovary and uterus were increased significantly; (7) the numbers of mature oocytes in fallopian tubes were increased significantly. The results show that kinetin can protect ovary and uterus against oxidative damage, prevent low estrogen secretion caused by ovarian oxidative damage, shorten the estrous cycle in mice, and eventually maintain ovarian and uterine vitalities.
