Irpex lacteus polysaccharide exhibits therapeutic potential for ovarian fibrosis in PCOS rats via the TGF-β1/smad pathway

Zhou, Yumin; Wu, Yongjiang; Chong, Chee Keong; Zhong, Sen; Wang, Zi‐Xian; Xiao, Qin; Liu, Zhiqiang; Liu, Junyang; Song, Jia‐Le

doi:10.1016/j.heliyon.2023.e18741

Cited by 2 publications

(1 citation statement)

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“…Oxidative stress is considered one of the risk factors for PCOS (Khodaeifar et al., 2018 ; Zhou et al., 2023 ). It has been reported that PCOS patients have decreasing levels of glutathione peroxidase (GPx) and SOD (Furat Rencber et al., 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Sinapic acid modulates oxidative stress and metabolic disturbances to attenuate ovarian fibrosis in letrozole‐induced polycystic ovary syndrome SD rats

Lan,

Dong,

Zhang

et al. 2024

Food Science & Nutrition

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Sinapic acid (SA) is renowned for its many pharmacological activities as a polyphenolic compound. The cause of polycystic ovary syndrome (PCOS), a commonly encountered array of metabolic and hormonal abnormalities in females, has yet to be determined. The present experiment was performed to evaluate the antifibrotic properties of SA in rats with letrozole‐induced PCOS‐related ovarian fibrosis. SA treatment successfully mitigated the changes induced by letrozole in body weight (BW) (p < .01) and relative ovary weight (p < .05). Histological observation revealed that SA reduced the number of atretic and cystic follicles (AFs) and (CFs) (p < .01), as well as ovarian fibrosis, in PCOS rats. Additionally, SA treatment impacted the serum levels of sex hormones in PCOS rats. Luteinizing hormone (LH) and testosterone (T) levels were decreased (p < .01, p < .05), and follicle‐stimulating hormone (FSH) levels were increased (p < .05). SA administration also decreased triglyceride (TG) (p < .01) and total cholesterol (TC) levels (p < .05) and increased high‐density lipoprotein cholesterol (HDL‐C) levels (p < .01), thereby alleviating letrozole‐induced metabolic dysfunction in PCOS rats. Furthermore, SA treatment targeted insulin resistance (IR) and increased the messenger RNA (mRNA) levels of antioxidant enzymes in the ovaries of PCOS rats. Finally, SA treatment enhanced the activity of peroxisome proliferator‐activated receptor‐γ (PPAR‐γ), reduced the activation of transforming growth factor‐β1 (TGF‐β1)/Smads, and decreased collagen I, α‐smooth muscle actin (α‐SMA), and connective tissue growth factor (CTGF) levels in the ovaries of PCOS rats. These observations suggest that SA significantly ameliorates metabolic dysfunction and oxidative stress and ultimately reduces ovarian fibrosis in rats with letrozole‐induced PCOS.

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Section: Discussionmentioning

confidence: 99%