Hyperoside attenuates pregnancy loss through activating autophagy and suppressing inflammation in a rat model

Abstract

AimsRecurrent pregnancy loss (RPL) is one of the most common obstetrical diseases, which is a manifestation of antiphospholipid syndrome (APS) with no effective therapy methods. Autophagy and inflammatory responses both play an important role in the pathogenesis of RPL and hyperoside has been demonstrated to have multifarious bioactivities including enhancing autophagy and anti-inflammation. This study aims to investigate the effect of hyperoside on anticardiolipin (aCL)-IgG fractions-induced pregnancy loss. Main methodsIn the present study, the effect of hyperoside was evaluated in a rat model of pregnancy loss induced by aCL-IgG fractions isolated from serum of APS patients. The fetuses were counted and the placentas were weighted and the protein expressions of inflammation and autophagy were measured by western blot analysis. Key findingsTreatment with hyperoside (40 mg/kg) improved pregnancy outcome manifest as increasing the weight of fetuses and decreasing the fetal resorption rate. In addition, hyperoside treatment downregulated the expressions of phosphorylated mammalian target of rapamycin (mTOR), phosphorylated p70S6 Kinase (S6K) and inhibited the expressions of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and NF-kB p-p65 in pregnancy loss animal models. SignificanceHyperoside attenuated pregnancy loss through regulating mTOR/S6K and TLR4/MyD88/NF-kB signaling pathways, which may provide a potential drug candidate for recurrent pregnancy loss therapy.