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Corilagin decreases insulin resistance in polycystic ovary syndrome rat model through regulating AMPK/GSK3β pathway

BACKGROUND: This study aims to explore the effects of Corilagin on insulin resistance (IR) of polycystic ovary syndrome (PCOS) and the underlying mechanisms. METHODS: The PCOS rat model was established by subcutaneously injected with dehydroepiandrosterone (DHEA) of 6 mg/kg/day. Body weight and ovar...

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Detalles Bibliográficos
Autores principales: Lv, Beili, Li, Xinrong, Wang, Haiyan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8798515/
https://www.ncbi.nlm.nih.gov/pubmed/35117690
http://dx.doi.org/10.21037/tcr.2020.04.27
Descripción
Sumario:BACKGROUND: This study aims to explore the effects of Corilagin on insulin resistance (IR) of polycystic ovary syndrome (PCOS) and the underlying mechanisms. METHODS: The PCOS rat model was established by subcutaneously injected with dehydroepiandrosterone (DHEA) of 6 mg/kg/day. Body weight and ovary weight were recorded. Serum glucose and insulin concentration were analyzed with commercial kits. The expression of adenosine monophosphate-activated protein kinase (AMPK) and glycogen synthase kinase 3β (GSK3β) was detected by Western blot. RESULTS: The results showed that DHEA could induce ovarian dysfunction of rats and Corilagin alleviated DHEA-induced ovarian dysfunction. Corilagin reduced DHEA-induced increase of serum glucose and insulin concentration. Corilagin increased the expression level of p-AMPK/AMPK and p-GSK3β/GSK3β of rat ovarian induced by DHEA. CONCLUSIONS: The present research reported the protective effects of Corilagin on PCOS, and demonstrated the protection effect was related to decreasing IR through regulating AMPK/GSK3β pathway.