Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
[Wuzi Yanzong Pill ameliorates diminished ovarian reserve in mice by inhibiting granulosa cell apoptosis via the TGF-β1/PI3K/Akt/mTOR pathway].
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Liang Yunteng, Gao Qian, Li Yueyi, Huang Jingyu, Liu Kailu, Hong Yanli, Zhou Huifang, Nie Xiaowei
Аннотация
OBJECTIVES: To investigate the efficacy of Wuzi Yanzong Pill (WZYZP) for improving diminished ovarian reserve (DOR) in mice and explore the underlying mechanism.
METHODS: Female C57BL/6J mice were randomly divided into control group, Tripterygium wilfordii polyglycoside-induced DOR model group, and two WZYZP groups treated with WZYZP at daily doses of 1.82 or 3.64 g/kg for 28 days (n=8). Ovarian index of the mice was calculated, hormone levels were detected with ELISA, and ovarian histopathological changes were observed using HE staining. RNA sequencing was performed to identify the key signaling pathways involved in WZYZP treatment for DOR. Network pharmacology analysis was used to predict the potential targets and pathways of WZYZP. Immunohistochemistry and Western blotting were used to detect ovarian expressions of the key proteins in the TGF‑β1/PI3K/Akt/mTOR pathway. Granulosa cell (GC) apoptosis levels were assessed with TUNEL staining and Western blotting. In addition, human GCs samples were collected from DOR patients for validating the expressions of the TGF‑β1/PI3K/Akt/mTOR pathway using Western blotting.
RESULTS: In the mouse models of DOR, WZYZP treatment significantly improved the ovarian index, increased anti-Müllerian hormone (AMH) and estradiol (E2) levels, decreased follicle stimulating hormone (FSH) level, alleviated ovarian pathologies, enhanced GC function, and reduced atretic follicles. RNA-seq revealed significant enrichment of the PI3K/Akt pathway after WZYZP treatment. Network pharmacology analysis suggested that the TGF‑β, PI3K‑Akt, and apoptosis pathways were the key pathways potentially targeted by WZYZP. WZYZP treatment significantly upregulated the expressions of TGF‑β1, PI3K, Akt, and mTOR in mouse ovarian tissues and inhibited GC apoptosis. Western blotting of human GCs further verified the down‑regulation of TGF‑β1/PI3K/Akt/mTOR pathway in DOR patients.
CONCLUSIONS: WZYZP improves ovarian reserve by upregulating the TGF‑β1/PI3K/Akt/mTOR signaling pathway and inhibiting excessive apoptosis of GCs.
METHODS: Female C57BL/6J mice were randomly divided into control group, Tripterygium wilfordii polyglycoside-induced DOR model group, and two WZYZP groups treated with WZYZP at daily doses of 1.82 or 3.64 g/kg for 28 days (n=8). Ovarian index of the mice was calculated, hormone levels were detected with ELISA, and ovarian histopathological changes were observed using HE staining. RNA sequencing was performed to identify the key signaling pathways involved in WZYZP treatment for DOR. Network pharmacology analysis was used to predict the potential targets and pathways of WZYZP. Immunohistochemistry and Western blotting were used to detect ovarian expressions of the key proteins in the TGF‑β1/PI3K/Akt/mTOR pathway. Granulosa cell (GC) apoptosis levels were assessed with TUNEL staining and Western blotting. In addition, human GCs samples were collected from DOR patients for validating the expressions of the TGF‑β1/PI3K/Akt/mTOR pathway using Western blotting.
RESULTS: In the mouse models of DOR, WZYZP treatment significantly improved the ovarian index, increased anti-Müllerian hormone (AMH) and estradiol (E2) levels, decreased follicle stimulating hormone (FSH) level, alleviated ovarian pathologies, enhanced GC function, and reduced atretic follicles. RNA-seq revealed significant enrichment of the PI3K/Akt pathway after WZYZP treatment. Network pharmacology analysis suggested that the TGF‑β, PI3K‑Akt, and apoptosis pathways were the key pathways potentially targeted by WZYZP. WZYZP treatment significantly upregulated the expressions of TGF‑β1, PI3K, Akt, and mTOR in mouse ovarian tissues and inhibited GC apoptosis. Western blotting of human GCs further verified the down‑regulation of TGF‑β1/PI3K/Akt/mTOR pathway in DOR patients.
CONCLUSIONS: WZYZP improves ovarian reserve by upregulating the TGF‑β1/PI3K/Akt/mTOR signaling pathway and inhibiting excessive apoptosis of GCs.