4.7 Article

Caffeic acid's role in mitigating polycystic ovary syndrome by countering apoptosis and ER stress triggered by oxidative stress

Journal

BIOMEDICINE & PHARMACOTHERAPY
Volume 166, Issue -, Pages -

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2023.115327

Keywords

Polycystic ovary syndrome (PCOS); Caffeic acid; Hyperandrogenemia; Oxidative stress; hypergly-cemia; Dehydroepiandrosterone (DHEA)

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This study investigated the therapeutic effect of caffeic acid on PCOS and its underlying molecular mechanism. The results showed that caffeic acid could inhibit oxidative stress and improve PCOS-related complications by modulating ER stress.
Polycystic ovary syndrome (PCOS) is a complex endocrine disorder that affects women of reproductive age, characterized by androgen-induced oxidative stress leading to several metabolic disorders. In this study, we investigated the potential therapeutic effect of caffeic acid on PCOS and its underlying molecular mechanism. We used a human ovarian granulosa cell line (KGN cells) induced by hydrogen peroxide (H2O2) to examine how caffeic acid influences the protein expression of oxidative stress-induced apoptosis-related markers. Our results indicate that caffeic acid significantly inhibits intracellular reactive oxygen species (ROS) generation and safe-guards KGN cells against oxidative stress. For the in vivo aspect of our study, female Sprague-Dawley (SD) rats were utilized to induce the PCOS model using dehydroepiandrosterone (DHEA). Caffeic acid was then administered to the rats for a duration of 6 weeks. The outcomes revealed that caffeic acid effectively improved irregular estrous cycles, fasting blood glucose levels, liver function, and lipid profiles in DHEA-induced PCOS rats. Additionally, it mitigated hyperandrogenism, enhanced steroidogenesis enzyme expression, and modulated apoptosis-related protein expression. Our findings strongly suggest that caffeic acid holds promising potential in reducing oxidative stress-induced damage and ameliorating PCOS-related complications by modulating ER stress.

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