Hyperoside Inhibits Endometrial Fibrosis and Inflammation by Targeting TGF-β/Smad3 Signaling in Intrauterine Adhesion Rats

Zheng-yan Zhu, Yu Song, Xuemei Chen, Huan Huang, Yuanping Xu, Lin Zhao
In: Revista Brasileira de Farmacognosia · 2022 · vol. 33(1) , pp. 89–94 · doi:10.1007/s43450-022-00283-5 · W4312134166
article OA: closed CC0
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-08 ⓘ

Hyperoside treatment alleviated endometrial fibrosis and inflammation in rats by repressing the activation of the TGF-β/Smad3 signaling pathway.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-08 ⓘ

This study examined whether hyperoside could reduce endometrial fibrosis and inflammation in a rat model of intrauterine adhesions, using 32 female Sprague Dawley rats assigned to groups with or without hyperoside and with dual injury to induce adhesions. In treated animals, Masson staining and Western blotting showed decreased endometrial fibrosis markers, while ELISA and RT-qPCR indicated reduced proinflammatory factor expression; hyperoside also repressed activation of the TGF-β/Smad3 signaling pathway. The authors’ main caveat is that effects were demonstrated in an animal adhesion model rather than in human disease or via direct mechanistic manipulation beyond pathway inhibition readouts. This paper is centrally about endometriosis — it targets endometrial fibrosis and inflammation in an intrauterine adhesion rat model, which is closely related to endometrial pathology relevant to endometriosis-related uterine remodeling.

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