Effects of resveratrol on autophagy and the expression of inflammasomes in a placental trophoblast oxidative stress model

We aim to investigate whether there is activation of NLRP1 and autophagy in trophoblast oxidative stress model. Resveratrol was taken to clarify its role in oxidative damage of placental trophoblasts. H2O2 was added to HTR-8/SVneo cell for 3 h, then the ROS level and apoptosis panel was performed. The levels of IL-1β, caspase-1, NLRP1, LC3 and Beclin-1 were detected. Resveratrol was added after 8 h, the ROS level and apoptosis rate were detected, the expression of IL-1β, caspase-1, NLRP1, LC3 and Beclin-1 were detected. 300 μmol/L H2O2 for 3 h is the optimum combination in establishing the oxidative stress injury model (P < 0.01). LDH, ROS and MDA level was increased, the activity of SOD, CAT were declined (P < 0.01). Apoptosis rate increased (P < 0.01). The expression of IL-1β, caspase-1, NLRP1, LC3 and Beclin-1 protein was higher (P < .01). Resveratrol (50 μmol/L) treatment for 8 h could improve the changes caused by H2O2, increase the survival rate of cells (P < 0.01), reduce the release of LDH, decrease the level of MDA, increase the level of SOD and CAT (P < 0.01). The expression of IL-1β, caspase-1, NLRP1, LC3 and Beclin-1 protein decreased (P < 0.01). Trophoblast oxidative damage model can be established under 300 μmol/L H2O2 for 3 h, the expression of NLRP1and autophagy after H2O2 treatment were detected. Resveratrol reduces apoptotic cells, thus ensuring the normal biological functions of trophoblasts. H2O2-induced oxidative stress damage model in HTR-8/SVneo cells can be successfully established under 300 μmol/L H2O2 for 3 h, resveratrol alleviates of H2O2-induced damage by its antioxidant and autophagy regulation function.