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绿原酸通过卵巢肾素-血管紧张素系统改善慢性不可预测应激诱导的卵巢储备功能下降。

Chlorogenic Acid Ameliorates Chronic Unpredictable Stress-Induced Diminished Ovarian Reserve Through Ovarian Renin-Angiotensin System.

作者信息

Qian Fei, Zhu Zhengyu, Luo Chao, Qi Ruofan, Wei Lun, Bo Le, Jiang Wangtao, Mao Caiping

机构信息

Reproductive Medicine Center, First Affiliated Hospital of Soochow University, Suzhou, China.

Department of Urology, First Affiliated Hospital of Soochow University, Suzhou, China.

出版信息

Mol Nutr Food Res. 2025 Mar;69(5):e202400814. doi: 10.1002/mnfr.202400814. Epub 2025 Jan 31.

DOI:10.1002/mnfr.202400814
PMID:39891261
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11874143/
Abstract

Chronic stress could impair ovarian reserve through hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis, leading to reduced oocyte quality and endocrine dysfunction. The ovarian renin-angiotensin system (OVRAS) modulates follicular development, and excessive activation of the ACE-AngII-AT1R axis increases oxidative stress, disrupting ovarian function. This study investigates OVRAS's role in chronic unpredictable stress (CUS)-induced diminished ovarian reserve (DOR) and explores the protective effects of chlorogenic acid (CGA). Female mice were subjected to CUS (10 intervention methods were randomly applied to mice according to low, medium, and high frequency) and CGA treatment. Hormone levels, estrous cycles, ovarian morphology, oxidative stress, and apoptosis were evaluated. Results demonstrated that CUS overactivated the ACE-AngII-AT1R axis, increasing oxidative stress and apoptosis in granulosa cells (GCs). CGA improved ovarian function, reduced oxidative stress, and downregulated ACE-AngII-AT1R axis activity. CGA may alleviate stress-induced DOR by mitigating oxidative stress and apoptosis via modulation of the ACE-AngII-AT1R axis.

摘要

慢性应激可通过下丘脑-垂体-肾上腺(HPA)轴的过度激活损害卵巢储备,导致卵母细胞质量下降和内分泌功能障碍。卵巢肾素-血管紧张素系统(OVRAS)调节卵泡发育,ACE-AngII-AT1R轴的过度激活会增加氧化应激,破坏卵巢功能。本研究调查OVRAS在慢性不可预测应激(CUS)诱导的卵巢储备功能减退(DOR)中的作用,并探讨绿原酸(CGA)的保护作用。对雌性小鼠进行CUS处理(根据低、中、高频率随机对小鼠应用10种干预方法)和CGA处理。评估激素水平、发情周期、卵巢形态、氧化应激和细胞凋亡。结果表明,CUS使ACE-AngII-AT1R轴过度激活,增加了颗粒细胞(GCs)中的氧化应激和细胞凋亡。CGA改善了卵巢功能,降低了氧化应激,并下调了ACE-AngII-AT1R轴的活性。CGA可能通过调节ACE-AngII-AT1R轴减轻氧化应激和细胞凋亡,从而缓解应激诱导的DOR。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5774/11874143/2f3dd406892a/MNFR-69-e202400814-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5774/11874143/e8bf9756026b/MNFR-69-e202400814-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5774/11874143/162d08dee73a/MNFR-69-e202400814-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5774/11874143/9b76a7b49d83/MNFR-69-e202400814-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5774/11874143/349dcfc71dde/MNFR-69-e202400814-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5774/11874143/2f3dd406892a/MNFR-69-e202400814-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5774/11874143/e8bf9756026b/MNFR-69-e202400814-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5774/11874143/162d08dee73a/MNFR-69-e202400814-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5774/11874143/9b76a7b49d83/MNFR-69-e202400814-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5774/11874143/349dcfc71dde/MNFR-69-e202400814-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5774/11874143/2f3dd406892a/MNFR-69-e202400814-g002.jpg

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