The effects of Mussel Adhesive Protein, COL III, and β-Glucan on Vaginal Mucosal Injury.

Authors

Tengfei Long, Miao Ding, Qiyue Hu, Junzhe Li, Jianda Ma, Yunfeng Sun

Published in

The international journal of biochemistry & cell biology. Pages 107033. Sep 20, 2026. Epub Sep 20, 2026.

Abstract

Vaginal mucosal inflammation (VMI) injury results in loss of epithelial integrity and mucosal injury, predisposing women to infections and reproductive complications; however, effective therapies that promote mucosal repair remain limited. Here, we investigated the effects of mussel adhesive protein (MAP), type III collagen (COL III), and β-glucan on the lipopolysaccharide (LPS)-induced VMI injury model. The VMI injury cellular model was constructed by using LPS-induced human vaginal epithelial cells. We optimized the concentration of the above three agents and evaluated the effects of MAP, COL III, and β-glucan on proliferation, migration, antioxidant capacity, and inflammatory factors. The results suggested that the MAP had no effect on migration and proliferation, and no further investigation of the MAP was performed, as this result indicated that the MAP failed to meet the main purpose of the present study. The combination of COL III and β-glucan promoted migration and proliferation compared with the control group (P < 0.05, as indicated by scratch closure). However, none of the treatments significantly alter inflammatory cytokine levels or antioxidant activity under the present experimental conditions (P > 0.05). Transcriptomic profiling revealed that treatments of COL III and β-glucan were associated with distinct transcriptional changes enriched in stress adaptation and tissue repair-related pathways, accompanying the enhanced epithelial migration and proliferation, without markedly affecting classical inflammatory cytokine expression. These findings suggest that COL III and β-glucan may promote epithelial repair and that the observed transcriptional alterations are associated with this response.

PMID:
42764126
Bibliographic data and abstract were imported from PubMed on 21 Sep 2026.

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