Protective effect of baicalein on mouse ovarian injury induced by triptolide / 中草药

ABSTRACT

Objective To investigate the effect of baicalein on mouse ovarian injury induced by triptolide. Methods Female healthy BALB/C mice were randomized into four groups. The mice in control group were given water contained 5% DMSO. The mice in model group were given 25 μg/kg triptolide orally. While the mice in baicalein treated groups were given 25 μg/kg triptolide plus 100 mg/kg and 500 mg/kg baicalein, respectively. On the 41st d of experiment, continuous vaginal smear were made to measure the sexual cycle of mice. On the 47th d, the superovulation experiment was carried out. On the 50th d, the mice were sacrificed to collect the ovaries. Ovaries were examined by hematoxylin and eosin (HE) staining, and the levels of follicles were counted. The levels of superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) in the ovarian tissue of each group were measured to evaluate the level of oxidative stress. Western blotting assay was performed to measure the expression levels of thioredoxin reductase (TrxR), thioredoxin (Trx), glutathione reductase (GR), and GSH-Px. Results Triptolide significantly induced ovarian damage, reduced the number of follicles, induced ovarian interstitial connective tissue regional osteoporosis, and decreased the activities of SOD and GSH-Px, while increased the content of MDA. On the contrary, when adding baicalein, the mice ovary development was obviously improved. The follicle cell number increased, and the connective tissue in interstitial region of ovary was well-stacked. The activity of SOD and GSH-Px in ovarian tissue was increased and the content of MDA was decreased. Western Blotting results showed that the expression levels of TrxR in model group mice were significantly down-regulated compared with those of control group. However, compared with control group, the expression levels of TrxR were significantly up-regulated by baicalein treatment. Conclusion Baicalein can enhance the anti-oxidative ability of mouse ovarian tissue by up-regulating TrxR expression, and may play an important role in the protection of ovarian injury induced by triptolide.