Taxifolin attenuates ischemia-reperfusion induced oxidative ovarian damage in rats

Objective:To investigate preventive effects of taxifolin on ischemia-reperfusion induced oxidative ovarian damage in rats.Methods:A total of 18 female Wistar albino rats were randomly and equally divided into three groups:the sham group,the ovarian ischemia reperfusion group,and the 50 mg/kg taxifolin+ovarian ischemia reperfusion group.The ovarian ischemia reperfusion and taxifolin+ovarian ischemia reperfusion groups were exposed to ischemia for 2 h and then followed by two-hour reperfusion protocol.Biochemical and histopathologic examinations were performed on the extracted ovaries.Results:Levels of malondialdehyde and cyclooxygenase-2 were increased,while reduced-glutathione and cyclooxygenase-1 were decreased in the ovarian ischemia reperfusion group.However,these values were reversed in the taxifolin+ovarian ischemia reperfusion group.Similarly,the number of primordial and developing follicules decreased in the ovarian ischemia reperfusion group,while they were within normal range in the taxifolin+ovarian ischemia reperfusion group.Conclusions:Ischemia followed by reperfusion leads to oxidative stress-related ovarian injury,and taxifolin may be useful for protecting ovarian tissue from such injury.

Betulinic acid protects against ovarian impairment by decreasing F-2 toxin-induced oxidative stress and inflammation associated with the downregulation of p38 expression in mice

F-2 toxin is an estrogenic mycotoxin that causes reproductive disorders in animals.Betulinic acid(BA)is a natural pentacyclic lupane-structure triterpenoid that has diverse pharmacological activities.In this study,the antioxidative and anti-inflammatory effects of BA and its underlying mechanism are explored in F-2 toxin-triggered mouse ovarian damage.We found that BA alleviated the F-2 toxin-induced ovarian impairment by stimulating follicle growth,reducing inflammatory cell infiltration,repairing damaged mitochondria and endoplasmic reticulum.Simultaneously,BA not only reversed F-2 toxin-induced reduction of follicle stimulating hormone(FSH)and luteinizing hormone(LH)levels in the serum,but also restrained the protein expression of the estrogen receptors a(ERa)and ERβ.Moreover,BA restored the balance of F-2 toxin-induced ovarian redox system disorders.Subsequently,we found that 0.25 mg/kg BA played an anti-inflammatory role in the F-2 toxin-induced ovarian impairment by decreasing interleukin-1β(IL-1β).IL-6,and tumor necrosis factor-α(TNF-α)mRNA expression,as well as inhibiting p38 protein expression.These data demonstrated that BA exerts its protective effect on F-2 toxin-induced ovarian oxidative impairment and inflammation by inhibiting p38 expression,which implies a natural product-based medicine to ameliorate F-2 toxin-caused female reproductive toxicity and provides a detoxifying method for food contaminated by mycotoxin.