The protective effect of vinpocetine against Estradiol-benzoate induced cervical hyperkeratosis in female rats via modulation of SIRT1/Nrf2, and NLRP3 inflammasome

Remon Roshdy Rofaeil, Reham H. Mohyeldin, Ehab E Sharata, Mina Ezzat Attya, Hany Essawy, Osama Ibrahim, Walaa Yehia Abdelzaher
In: Scientific Reports · 2024 · vol. 14(1) , pp. 19171 · doi:10.1038/s41598-024-69431-2 · PMID:39160173 · W4401705672
article OA: gold CC0 ⤵ 2 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Vinpocetine mitigated estradiol benzoate-induced cervical hyperkeratosis in rats by reducing inflammation and oxidative stress through modulation of SIRT1/Nrf2 and NLRP3 inflammasome pathways.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

This study examined whether vinpocetine could prevent estradiol-benzoate–induced cervical hyperkeratosis in female rats. Estradiol benzoate was administered intramuscularly for 4 weeks to induce hyperkeratosis, with or without concomitant oral vinpocetine, and cervical tissues were assessed for oxidative stress markers (MDA, NOx, GSH), inflammatory cytokines (TNF-α, IL-18, IL-1β), and protein expression in the NLRP3/GSDMD/caspase-1 and SIRT1/Nrf2 pathways, alongside histopathology. Estradiol benzoate increased oxidative stress and inflammatory mediators and upregulated NLRP3/caspase-1 while reducing GSH, SIRT1, and Nrf2, whereas vinpocetine significantly alleviated these biochemical and histological changes. The paper explicitly limits interpretation to this rat model and dosing regimen, since it reports preventive effects and mechanistic associations rather than clinical outcomes. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

The current study was assigned to determine the putative preventive role of vinpocetine (VIN) in cervical hyperkeratosis (CHK) in female rats. Estradiol Benzoate (EB) was utilized in a dose f (60 μg/100 g, i.m) three times/week for 4 weeks to induce cervical hyperkeratosis. VIN was administered alone in a dose of (10 mg/kg/day, orally) for 4 weeks and in the presence of EB. Levels of malondialdehyde (MDA), total nitrites (NOx), reduced glutathione (GSH), interleukin-18 (IL-18), IL-1β, tumor necrosis factor-alpha (TNF-α) were measured in cervical tissue. The expression of NLRP3/GSDMD/Caspase-1, and SIRT1/Nrf2 was determined using ELISA. Cervical histopathological examination was also done. EB significantly raised MDA, NOx, TNF-α, IL-18, IL-1β, and GSDMD and up-regulated NLRP3/Caspase-1 proteins. However, GSH, SIRT1, and Nrf2 levels were reduced in cervical tissue. VIN significantly alleviates all biochemical and histopathological abnormalities. VIN considerably mitigates EB-induced cervical hyperkeratosis via NLRP3-induced pyroptosis and SIRT1/Nrf2 signaling pathway.

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