Mechanism of selenium supplementation in preventing and treating retained placenta in yaks: selenium inhibits LPS-induced apoptosis and inflammatory injury of YEECs via the PI3K/AKT/NF-κB signaling pathway

Selenium (Se) deficiency in yaks usually causes retained placenta (RP) during parturition. Currently, the mechanism of Se supplementation in preventing and treating RP remains unclear. This study aimed to clarify the effects of Se on apoptosis and inflammatory injury in yak endometrial epithelial cells (YEECs). ICP-MS measured serum Se concentrations in yaks with normal parturition (NP) and with RP. RT-qPCR and WB quantified expression of genes and proteins involved in apoptosis, inflammation, and tissue repair in the corresponding placental tissues. Following LPS-induced apoptotic and inflammatory injury, YEECs were treated with different Na2SeO3 concentrations, changes in apoptosis and inflammatory injury were then assessed by RT-qPCR, WB, TUNEL, and scratch assays. The results showed that the Se concentration in the serum of yaks with RP was significantly lower than that in yaks with NP (P < 0.01). The expression of genes and proteins related to apoptosis and tissue repair in the placental tissue of yaks with RP was significantly decreased, while the expression of inflammatory factors was significantly increased (P < 0.05). Na2SeO3 at 1, 2, and 4 μM significantly reduced YEECs apoptosis and inflammatory factor expression while enhancing the repair capacity of injury cells. The 2 μM concentration produced the largest effect (P < 0.05). In addition, 2 μM Na2SeO3 could significantly inhibit the activation of the PI3K/AKT/NF-κB pathway (P < 0.01). In conclusion, Se inhibited LPS-induced apoptosis and inflammatory injury of YEECs through the PI3K/AKT/NF-κB signaling pathway. This study provides new scientific evidence for elucidating the mechanism by which selenium supplementation prevents and treats RP in yaks.