Selenium ameliorates aflatoxin B1-induced uterine injury in female mice and necrosis of human endometrial microvascular endothelial cells.

Abstract

This study aimed to observe the effects of Selenium (Se) on aflatoxin B1 (AFB1)-induced uterine injury in female mice and necrosis of human endometrial microvascular endothelial cells (HEMECs). Fifty female mice were randomly divided into control group; AFB1 group; Se group (0.2 mg/kg each day); AFB1 + Se group; and positive control group. After continuous treatment for 30 days, uterine tissues were harvested, which were used for hematoxylin and eosin (H&E) staining. Necrosis-related proteins including RIPK1, RIPK3, and MLKL were examined in uterine tissues using western blot and immunohistochemistry. HEMECs were treated with different concentrations of AFB1 or Se, which were used for selecting the optimal concentrations. RIPK1, RIPK3 and MLKL expression was detected in HEMECs exposed to AFB1 and/or Se via western blot and immunofluorescence. H&E staining results showed that AFB1 induced uterine injury of female male, which was ameliorated by Se treatment. According to western blot and immunohistochemistry, RIPK1, RIPK3, and MLKL expression was distinctly increased in uterine tissues of AFB1-treated mice, which was decreased by Se treatment. Cell viability of HEMECs was gradually lowered as the concentrations of AFB1and Se increased. A 10-μM AFB1 exposure significantly increased RIPK1, RIPK3, and MLKL expression in HEMECs, which was improved following co-treatment with 5-μM Se. Thus, our findings revealed that Se may ameliorate AFB1-induced uterine injury in female mice and necrosis of HEMECs.