Intraperitoneal Fetuin-A Modulates HMGB1-Associated Inflammatory Remodeling in Experimental Endometriosis

Selim Afşar, Özgür Bulmuş, Çamili FE, Mustafa Hilmi Yaranoğlu, Mine İslimye Taşkın, Ayla Solmaz Avcıkurt, Gürhan Güney, Ezgi Tolu Cenk, Hilmi Bolat, Ceyda Sancaklı Usta, Merve Akış, Akın Usta, Gülay Turan
In: Biomedicines · 2026 · vol. 14(10) , pp. 2149 · doi:10.3390/biomedicines14102149 · W7214126928
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Intraperitoneal Fetuin-A reduced lesion area and systemic inflammation while modulating HMGB1 mRNA and remodeling markers in a rat model of endometriosis.

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Abstract

Background/Objectives: Endometriosis is a chronic inflammatory disorder characterized by ectopic endometrial-like lesions, inflammatory activation, angiogenesis, and tissue remodeling. Fetuin-A has been implicated in inflammatory regulation; however, its effects on HMGB1 mRNA expression and lesion-remodeling markers in endometriosis remain unclear. This study investigated whether intraperitoneal Fetuin-A is associated with changes in systemic inflammation and lesion-associated remodeling in a surgically induced rat model of endometriosis. Methods: After confirmation of viable endometriotic implants, female Wistar albino rats received intraperitoneal Fetuin-A or saline. Serum IL-1β, IL-6, TNF-α, and AMH levels were measured. Endometriotic implants were evaluated by qRT-PCR for HMGB1 and OPN mRNA expression and by immunohistochemistry for Fetuin-A, p62/SQSTM1, caspase-3, VEGF, OPN, and SOD1. Results: For the primary lesion-area endpoint, Fetuin-A treatment remained associated with significantly lower post-treatment lesion area after adjustment for baseline lesion area. Compared with saline, Fetuin-A treatment significantly reduced serum IL-1β, IL-6, and TNF-α concentrations and was associated with lower AMH levels. In endometriotic implants, Fetuin-A was associated with marked downregulation of HMGB1 mRNA expression, whereas OPN mRNA was modestly increased. Immunohistochemistry showed increased Fetuin-A, p62/SQSTM1, caspase-3, and SOD1 staining, together with reduced VEGF and OPN staining after Fetuin-A treatment. Conclusions: Intraperitoneal Fetuin-A attenuated experimental endometriosis, with a significant baseline-adjusted reduction in the primary lesion-area endpoint, systemic inflammatory suppression, and reduced HMGB1 mRNA expression, accompanied by changes in angiogenesis-, oxidative stress-, apoptosis-, autophagy-, and remodeling-associated markers. Because HMGB1 protein/release, RAGE/TLR4/NF-κB signaling, and specific fibrosis markers were not assessed, these findings should not be interpreted as direct HMGB1 pathway inhibition or definitive anti-fibrotic activity. Overall, these results support further mechanistic studies evaluating Fetuin-A as a potential modulator of inflammatory and lesion-remodeling processes in endometriosis.

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