Resveratrol attenuates hydrogen peroxide-induced injury of rat ovarian 1 granulosa-lutein cells by resisting oxidative stress via the SIRT1/Nrf2/ARE 2 signaling pathway | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Resveratrol attenuates hydrogen peroxide-induced injury of rat ovarian 1 granulosa-lutein cells by resisting oxidative stress via the SIRT1/Nrf2/ARE 2 signaling pathway Minghui Cai, Jiao Wang, Haijuan Sun, Qi Guo, Chi Zhang, Haixu Yao, and 3 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-1663439/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background : The ovarian granulosa-lutein cells injury and apoptosis induced by oxidative stress may be responsible for female luteal phase deficiency. The antioxidant function of resveratrol has been confirmed, however, its effect on the expression of antioxidant enzymes and regulatory mechanism in ovarian granulosa-lutein cells remains unclear. Results : The H2O2 treatment induced the primary ovarian granulosa-lutein cells injury shown as decreased cell viability, impaired cellular morphology, decreased levels of progesterone and estradiol. The H2O2 treatment also exacerbated cell apoptosis demonstrated as more apoptotic cells stained by Hoechst staining, decreased level of anti-apoptosis protein Bcl-2 and increased level of pro-apoptosis protein Bax. These effects of cell injury and apoptosis induced by H2O2 can be ameliorated by resveratrol. Resveratrol also alleviated oxidative stress induced by H2O2 supported by decreased superoxide anion and cellular total ROS, decreased levels of malondialdehyde and protein carbonyl, increased total antioxidant capacity and biological activity of SOD. Western blot results demonstrated resveratrol reversed the H2O2-induced decrease in levels of antioxidant enzymes containing ARE sequences and activated SIRT1/Nrf2 pathway. Further treatment by siRNA-Nrf2 suggested resveratrol was unable to activate the expression of antioxidant enzymes under a condition of inhibition of Nrf2. Conclusions : In conclusion, these results indicated that resveratrol attenuated oxidative stress to protect H2O2-induced rat ovarian granulosa-lutein cells injury and apoptosis via SIRT1/Nrf2/ARE signaling pathway. Ovarian granulosa-lutein cells resveratrol oxidative stress SIRT1/Nrf2/ARE signaling pathway Full Text Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-1663439","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":106671449,"identity":"b3a7b0d5-1226-4379-a2c8-6cb683699bf0","order_by":0,"name":"Minghui Cai","email":"","orcid":"","institution":"Harbin Medical University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Minghui","middleName":"","lastName":"Cai","suffix":""},{"id":106671450,"identity":"89c7f237-c8d9-41ce-bb62-5b41b15760d6","order_by":1,"name":"Jiao Wang","email":"","orcid":"","institution":"Harbin Medical 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