Histology and histopathology · 2025
Pachymic acid ameliorates polycystic ovary syndrome via inactivating Akt/ERK signaling.
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Ji Dongmei, Zhang Chunhua, Fang Fang, Yi Yuanyuan
Аннотация
OBJECTIVE: Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder that adversely affects women's health and quality of life. Pachymic acid (PA), a bioactive ingredient from Poria cocos (Schw.) Wolf, has demonstrated protective effects against PCOS in a murine model. This study aims to investigate the underlying mechanism by which PA exerts protective effects against PCOS.
METHODS: Female Sprague-Dawley rats were treated with letrozole to induce PCOS. The ovarian granulosa cell line (KGN) was exposed to lipopolysaccharide (LPS) to mimic PCOS in vitro. Hematoxylin-eosin staining and TUNEL assay were used for ovarian histological analysis. The cell counting kit-8 assay was used to assess the viability of KGN cells. Flow cytometry was used for in vitro cell apoptosis analysis. Western blotting revealed molecular protein expression levels in rat ovaries and KGN cells.
RESULTS: PA attenuated LPS-induced lactate dehydrogenase release (p<0.01), reduced the cell apoptosis rate (p<0.001), Bax, and cleaved-caspase3 protein expression (p<0.001), and increased Bcl-2 protein expression (p<0.01) in KGN cells. PA attenuated letrozole-induced increases in testosterone (p<0.01), luteinizing hormone (p<0.01), and estradiol levels (p<0.05) and decreases in progesterone levels (p<0.05) in PCOS rats. PA promoted corpus luteum formation (p<0.001) and reduced the number of cystic follicles and cell apoptosis (p<0.001) in PCOS rats. PA blocked Akt and ERK signaling transduction in PCOS rats and KGN cells (p<0.001).
CONCLUSION: PA protects against PCOS and attenuates cell apoptosis by inactivating Akt and ERK signaling.
METHODS: Female Sprague-Dawley rats were treated with letrozole to induce PCOS. The ovarian granulosa cell line (KGN) was exposed to lipopolysaccharide (LPS) to mimic PCOS in vitro. Hematoxylin-eosin staining and TUNEL assay were used for ovarian histological analysis. The cell counting kit-8 assay was used to assess the viability of KGN cells. Flow cytometry was used for in vitro cell apoptosis analysis. Western blotting revealed molecular protein expression levels in rat ovaries and KGN cells.
RESULTS: PA attenuated LPS-induced lactate dehydrogenase release (p<0.01), reduced the cell apoptosis rate (p<0.001), Bax, and cleaved-caspase3 protein expression (p<0.001), and increased Bcl-2 protein expression (p<0.01) in KGN cells. PA attenuated letrozole-induced increases in testosterone (p<0.01), luteinizing hormone (p<0.01), and estradiol levels (p<0.05) and decreases in progesterone levels (p<0.05) in PCOS rats. PA promoted corpus luteum formation (p<0.001) and reduced the number of cystic follicles and cell apoptosis (p<0.001) in PCOS rats. PA blocked Akt and ERK signaling transduction in PCOS rats and KGN cells (p<0.001).
CONCLUSION: PA protects against PCOS and attenuates cell apoptosis by inactivating Akt and ERK signaling.