基于T1R2/3-mTORC1通路探讨3-DG抑制子宫内膜基质细胞蜕膜化及补肾健脾方的干预作用OA

Objective:To investigate the effect of 3-deoxyglucosone(3-DG)on the decidualization of human endo-metrial stromal cells(hESCs)and the intervention mechanism of Bushen Jianpi formula,with a focus on the role of the sweet taste receptor T1R2/3-mTORC1 signaling pathway in the regulation of aerobic glycolysis.Methods:hESCs were divided into non-decidualized induction group,decidualized induction group,sweet taste receptor inhibitor group,3-DG intervention group,and 3-DG+Bushen Jianpi formula group.Decidualization was induced with 1 μmol/L MPA combined with 0.5 mmol/L 8-Br-cAMP for 6 consecutive days.The levels of decidualization markers IGFBP-1 and PRL were detected by ELISA;Lactate levels were measured by colorimetric method;the mRNA expression levels of aerobic glycolysis rate-limiting enzymes(HK2,PKM2,LDHA),sweet taste receptors(T1R2,T1R3),and mTORC1 were detected by qPCR.Results:Compared with the non-decidualized group,the decidualized induction group showed significantly increased mRNA expression of T1R2,T1R3,mTORC1,HK2,PKM2,and LDHA,as well as significantly elevated lactate levels(P＜0.05).Compared with the decidualized induction group,both the sweet taste receptor inhibitor group and the 3-DG intervention group exhibited significantly decreased mRNA expression of the above genes,along with significantly reduced lactate levels and decidualization markers IGFBP-1 and PRL(P＜0.05).Compared with the 3-DG intervention group,the 3-DG+Bushen Jianpi formula group showed significantly increased mRNA expression of the above genes and lactate levels,as well as significantly improved decidualization markers(P＜0.05).Conclusion:The T1R2/3-mTORC1 signaling pathway is activated during decidualization and pro-motes aerobic glycolysis.3-DG impairs hESCs decidualization by inhibiting this pathway.Bushen Jianpi formula can partially reverse the inhibitory effect of 3-DG and restore decidualization-related gene expression and aerobic glycoly-sis levels.