平冲降逆方经miR-199a-3p/mTOR信号通路调控子宫内膜异位症大鼠异位病灶自噬的研究OA

Objective To investigate the potential mechanism of Pingchong Jiangni Formula(平冲降逆方,PCJNF)in alleviating endometriosis(EMs)in a rat model,focusing on its regulation of the miR-199a-3p/mechanistic target of rapamycin(mTOR)signaling pathway.Methods Forty female Sprague-Dawley(SD)rats were randomly divided into a sham-operated group,an EMs model group,a PCJNF-treated group,and a gestrinone-treated group.EMs was induced via autologous endometrial transplantation,while the sham-operated group underwent laparotomy only.Upon successful modeling,animals received daily oral gavage for 21 days:the PCJNF group received PCJNF(7.56 g·kg⁻¹),the gestrinone group received gestrinone suspension(0.26 mg·kg⁻¹),and the sham and model groups received an equivalent volume of saline.Ectopic lesions were harvested,and their mass and volume were measured.Histopathological changes were evaluated by hematoxylin-eosin staining(HE).The expression of autophagy-related factors(Beclin1,LC3 Ⅱ/LC3 I),miR-199a-3p,and mTOR in ectopic lesions was detected by immunohistochemistry(IHC),Western blot(WB),and quantitative reverse transcription polymerase chain reaction(RT-qPCR),respectively.Results Compared with the model group,PCJNF treatment significantly reduced the mass and volume of ectopic lesions(P<0.05).Histopathological examination showed reduced epithelial and stromal cell disorganization and inflammatory cell infiltration in the ectopic endometrium.The protein expression of Beclin1 and the LC3 Ⅱ/LC3 Ⅰ ratio were significantly increased(P<0.05),while mTOR protein expression was significantly decreased(P<0.01)in the PCJNF group.Concurrently,the expression level of miR-199a-3p was significantly upregulated(P<0.001).Conclusion The therapeu‑tic effect of PCJNF against EMs may be associated with its modulation of the miR-199a-3p/mTOR signaling pathway in ectopic endome‑trial tissue,thereby influencing autophagic activity and ameliorating the pathological progression of EMs.