Objective To investigate the effects of alfentanil on the endometrial repair and PI3K/Akt signaling pathway in endometrial hemorrhage model rats.

Methods Among 68 SPF-grade female SD rats, 17 were randomly selected as the control group, and the rest were used to establish the endometrial bleeding model rats. After successful modeling, they were divided into the afentanil group (16 rats), model group (17 rats) and afentanil + NVP-BEZ235 group (15 rats). The uterine bleeding volume, uterine morphology, pathological changes, coagulation function, sex hormones, endometrial restoration-related cytokines, endometrial pathological damage, microvessel density and protein expressions of PI3K, Akt and p-Akt were compared among all groups.

Results Compared with the control group, the endometrium in the model group was shorter in morphology and thicker, and the uterine tissue had more villi, decidua, edema and congestion, as well as a large number of defects. The uterine morphology and pathological changes in the afentanil group were significantly improved compared with the model group. However, in the afentanil + NVP-BEZ235 group, after adding NVP-BEZ235 to rats, the therapeutic effect of afentanil was reversed, and the uterine morphology and endometrial injury were aggravated. Compared with the model group and afentanil + NVP-BEZ235 group, the Akt protein, tumor necrosis factor (TNF) -α, PI3K protein, thromboplastin time (APTT), p-Akt protein, interleukin (IL) -1β, thromboplastin time (TT), fibrotic area, uterine bleeding volume, luteinizing hormone (LH), prothrombin time (PT) and follicle-stimulating hormone (FSH) in the afentanil group decreased (P ＜ 0.05), while the number of glands, progesterone (P), endometrial thickness, plasma fibrinogen (FIB), microvessel density (MVD) and estradiol (E2) levels increased (P ＜ 0.05).

Conclusions Alfentanil can promote the endometrial repair in rat models of endometrial bleeding, reduce the amount of uterine bleeding, improve the coagulation function, sex hormones and cytokines related to endometrial repair, and reduce endometrial pathological damage. The mechanism may be related to regulating the expression of proteins related to the PI3K/Akt signaling pathway.