Su Jing, Cheng Jie, Sun Hai-Xiang, Diao Zhen-Yu, Zhen Xin, Yang Jun, Ding Li-Jun, Hu Ya-Li
Center for Reproductive Medicine, The Affiliated Nanjing Drum Tower Hospital of Nanjing University Medical School, Nanjing City, China.
Birth Defects Res B Dev Reprod Toxicol. 2014 Jun;101(3):283-91. doi: 10.1002/bdrb.21111. Epub 2014 May 15.
This study was carried out to investigate the impact of tripterygium glycosides (TGs) on ovarian function of female rats in vitro and in vivo. In vitro studies showed that TG induced cells decrease at G1 phase and inhibited cell proliferation in rat granulosa cells. In vivo, female rats were intragastrically administered with TG at the dose of 60 mg/kg/day for consecutive 50 days. TG caused a prolonged estrous cycle, and a significant reduction in ovarian index, serum E2 level, and numbers of secondary and antral follicles (p < 0.05) in these rats. A significant reduction of viable embryos was demonstrated in TG-treated female rats after mating (p < 0.01). Further, we observed observed the reduced expression level of TGF-β1 after TG treatment in vitro and in vivo. Moreover, the expression of Smad2 and AKT was also decreased after TG treatment. These results suggest that TG can impair ovarian function through Smads-mediated TGF-β1 signal pathway.
本研究旨在探讨雷公藤多苷(TGs)对雌性大鼠卵巢功能的体内外影响。体外研究表明,TG可诱导大鼠颗粒细胞在G1期细胞减少并抑制细胞增殖。在体内,雌性大鼠连续50天以60mg/kg/天的剂量灌胃给予TG。TG导致这些大鼠的动情周期延长,卵巢指数、血清E2水平以及次级卵泡和窦状卵泡数量显著降低(p<0.05)。与TG处理的雌性大鼠交配后,可观察到存活胚胎数量显著减少(p<0.01)。此外,我们观察到在体外和体内TG处理后TGF-β1的表达水平降低。而且,TG处理后Smad2和AKT的表达也降低。这些结果表明,TG可通过Smads介导的TGF-β1信号通路损害卵巢功能。