Bletilla striata polysaccharide‑zinc complex ameliorates ulcerative colitis by modulating endoplasmic reticulum stress-associated autophagy and apoptosis

The mechanistic basis for the therapeutic action of Bletilla striata polysaccharide‑zinc complex (BSP-Zn) against ulcerative colitis (UC) remains poorly defined. This study aimed to determine whether the compound's therapeutic effects involve the regulation of the endoplasmic reticulum stress (ERS), autophagy, and apoptosis axis. BSP-Zn was synthesized, characterized, and then administered to DSS-induced UC mice at doses of 200 and 400 mg/kg/d, alongside BSP and 5-ASA controls. In vivo, BSP-Zn treatment dose-dependently ameliorated colonic pathological damage and suppressed the production of pro-inflammatory cytokines. An ERS model was established in HCT116 cells using thapsigargin (Tg). The results indicate that BSP-Zn alleviates UC by blocking activation of this endoplasmic reticulum stress pathway and attenuating autophagy and apoptosis responses. This work provides a preclinical mechanistic rationale for BSP-Zn as a potential therapeutic candidate for UC, warranting further translational investigation.