Cellular immunology · 2026
Astragalus polysaccharides ameliorate ulcerative colitis by targeting the HMGB1/TLR4 signaling axis to inhibit neutrophil extracellular trap formation.
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Tan Fang, Li Xianhe, Liu Shiyu, Yang Xin, Wang Zhuangmei, Meng Yong, Wu Qianqian, Huang Sihui, Chen Guangxia
Аннотация
PURPOSE: Ulcerative colitis (UC) pathogenesis involves neutrophil extracellular trap (NET) formation and intestinal barrier collapse. High mobility group box 1 (HMGB1) acts as a critical "alarmin," triggering neutrophil activation via the Toll-like receptor 4 (TLR4) axis. We investigated whether Astragalus polysaccharides (APS) could disrupt this "HMGB1-NETs" vicious cycle to treat UC.
METHODS: Severe colitis was induced in SD rats using 2,4,6-trinitrobenzene sulfonic acid (TNBS). Rats received APS (200, 400, 800 mg/kg), DNase I (to degrade NETs), or "APS + exogenous HMGB1" (functional rescue). Disease severity was assessed via Disease Activity Index (DAI) and histopathology. NETs were quantified by immunofluorescence (Cit-H3/MPO/PAD4 co-localization) and Western Blot.
RESULTS: TNBS induction was associated with marked NETosis, HMGB1 nucleocytoplasmic redistribution, and redox dysregulation. DNase I treatment supported the pathogenic contribution of NETs in this model. APS (800 mg/kg) ameliorated colitis, reduced NET-associated markers, and suppressed HMGB1/TLR4 signaling in colon tissue. Exogenous HMGB1 attenuated APS-mediated protection and reactivated NETosis-associated inflammatory changes. APS also partially restored redox homeostasis by normalizing catalase activity and improving SOD/GST activities.
CONCLUSION: APS ameliorates experimental UC in association with suppression of HMGB1/TLR4-linked NETosis and restoration of redox balance. These findings support APS as a potential regulator of NET-associated inflammation, while direct neutrophil-level and translational validation remains needed.
METHODS: Severe colitis was induced in SD rats using 2,4,6-trinitrobenzene sulfonic acid (TNBS). Rats received APS (200, 400, 800 mg/kg), DNase I (to degrade NETs), or "APS + exogenous HMGB1" (functional rescue). Disease severity was assessed via Disease Activity Index (DAI) and histopathology. NETs were quantified by immunofluorescence (Cit-H3/MPO/PAD4 co-localization) and Western Blot.
RESULTS: TNBS induction was associated with marked NETosis, HMGB1 nucleocytoplasmic redistribution, and redox dysregulation. DNase I treatment supported the pathogenic contribution of NETs in this model. APS (800 mg/kg) ameliorated colitis, reduced NET-associated markers, and suppressed HMGB1/TLR4 signaling in colon tissue. Exogenous HMGB1 attenuated APS-mediated protection and reactivated NETosis-associated inflammatory changes. APS also partially restored redox homeostasis by normalizing catalase activity and improving SOD/GST activities.
CONCLUSION: APS ameliorates experimental UC in association with suppression of HMGB1/TLR4-linked NETosis and restoration of redox balance. These findings support APS as a potential regulator of NET-associated inflammation, while direct neutrophil-level and translational validation remains needed.