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姜黄素通过上调大鼠模型中PPAR-γ表达和减轻氧化应激对多囊卵巢综合征的治疗作用。

The therapeutic effects of curcumin on polycystic ovary syndrome by upregulating PPAR-γ expression and reducing oxidative stress in a rat model.

作者信息

Zhang Wei, Peng Cong, Xu Lei, Zhao Yutai, Huang Chaolin, Lu Ling

机构信息

Department of Gynecology and Obstetrics, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu, China.

出版信息

Front Endocrinol (Lausanne). 2024 Nov 20;15:1494852. doi: 10.3389/fendo.2024.1494852. eCollection 2024.

DOI:10.3389/fendo.2024.1494852
PMID:39634175
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11614657/
Abstract

OBJECTIVE

Polycystic ovary syndrome (PCOS) is a prevalent endocrine and metabolic disorder that impacts 8-13% of women in their reproductive years. However, the drugs commonly used to treat PCOS are often prescribed off-label and may carry potential side effects. This study aimed to investigate the therapeutic effects of curcumin in a PCOS rat model.

MATERIALS AND METHODS

A PCOS rat model was established through daily subcutaneous injection of 60 mg/kg body weight of dehydroepiandrosterone (DHEA) for 21 days. The PCOS rats received a daily intragastric dose of 50 mg/kg body weight of curcumin for another 21 days. Ovarian morphological changes, estrous cycle changes, and hormone level changes were measured to evaluate the therapeutic effectiveness of curcumin in PCOS rats. Oxidative stress markers in the ovaries were analyzed to explore the mechanisms of curcumin in PCOS rats.

RESULTS

This study demonstrated that curcumin alleviated insulin resistance and significantly reduced serum levels of estradiol ( = 0.02), luteinizing hormone ( = 0.009), testosterone ( = 0.003), and the LH/FSH ratio ( = 0.008) in PCOS rats. Curcumin also restored normal ovarian morphology and the estrous cycle in these rats. Furthermore, curcumin treatment significantly decreased levels of oxidative stress markers, including malondialdehyde ( = 0.004) and reactive oxygen species ( = 0.005), while increasing antioxidant levels such as superoxide dismutase ( = 0.04), glutathione peroxidase ( = 0.002), and glutathione ( = 0.02) in ovarian tissues. Additionally, curcumin significantly upregulated PPAR-γ in the ovarian tissues of PCOS rats.

CONCLUSION

This study demonstrates that curcumin effectively restores ovarian morphology, hormone levels, and estrous cycles in PCOS rats. These effects may be linked to its ability to reduce oxidative stress in ovaries via the upregulation of PPAR-γ. Curcumin shows promise as a potential drug for the treatment of PCOS.

摘要

目的

多囊卵巢综合征(PCOS)是一种常见的内分泌和代谢紊乱疾病,影响8%至13%的育龄妇女。然而,常用于治疗PCOS的药物往往是超说明书用药,且可能有潜在副作用。本研究旨在调查姜黄素在PCOS大鼠模型中的治疗效果。

材料与方法

通过每天皮下注射60毫克/千克体重的脱氢表雄酮(DHEA),持续21天,建立PCOS大鼠模型。PCOS大鼠再连续21天每天接受50毫克/千克体重的姜黄素灌胃。测量卵巢形态变化、发情周期变化和激素水平变化,以评估姜黄素对PCOS大鼠的治疗效果。分析卵巢中的氧化应激标志物,以探索姜黄素在PCOS大鼠中的作用机制。

结果

本研究表明,姜黄素可减轻胰岛素抵抗,并显著降低PCOS大鼠血清中的雌二醇水平(P = 0.02)、黄体生成素水平(P = 0.009)、睾酮水平(P = 0.003)以及LH/FSH比值(P = 0.008)。姜黄素还使这些大鼠的卵巢形态和发情周期恢复正常。此外,姜黄素治疗显著降低了氧化应激标志物的水平,包括丙二醛(P = 0.004)和活性氧(P = 0.005),同时提高了卵巢组织中的抗氧化剂水平,如超氧化物歧化酶(P = 0.04)、谷胱甘肽过氧化物酶(P = 0.002)和谷胱甘肽(P = 0.02)。此外,姜黄素显著上调了PCOS大鼠卵巢组织中的PPAR-γ。

结论

本研究表明,姜黄素可有效恢复PCOS大鼠的卵巢形态、激素水平和发情周期。这些作用可能与其通过上调PPAR-γ降低卵巢氧化应激的能力有关。姜黄素有望成为治疗PCOS的潜在药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a497/11614657/ec4f8998446d/fendo-15-1494852-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a497/11614657/d2363dba5ee7/fendo-15-1494852-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a497/11614657/82b43e035ad6/fendo-15-1494852-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a497/11614657/ec4f8998446d/fendo-15-1494852-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a497/11614657/d2363dba5ee7/fendo-15-1494852-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a497/11614657/82b43e035ad6/fendo-15-1494852-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a497/11614657/ac6ca3630d30/fendo-15-1494852-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a497/11614657/8aff9ca6452a/fendo-15-1494852-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a497/11614657/ec4f8998446d/fendo-15-1494852-g005.jpg

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PPAR-γ promotes the polarization of rat retinal microglia to M2 phenotype by regulating the expression of CD200-CD200R1 under hypoxia.过氧化物酶体增殖物激活受体-γ 通过调节缺氧条件下 CD200-CD200R1 的表达促进大鼠视网膜小胶质细胞向 M2 表型极化。
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