Biochemistry and biophysics reports · 2026
Ononin combined with Lactobacillus paracasei alleviates DSS-induced ulcerative colitis by ferroptosis via inhibiting JAK2/STAT3 signaling pathway.
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Huang Mei, Yang Feng, Song Ju-Cai, Wang Xue, Jiao Pan-Pan, Kang Meng-Jie, Guo Qian-Qian, Si Liang-Zhu, Zhang Shu-Han, Luo Lin-Shan, Li Yong-Wei, Zhang Wei, Gong Yue-Sheng, Dong Lei
Аннотация
BACKGROUND: Ulcerative colitis (UC) is a chronic inflammatory bowel disease with a complex pathogenesis and limited treatment options. This study aimed to evaluate the therapeutic effect of Ononin combined with Lactobacillus paracasei in a dextran sulfate sodium (DSS)-induced murine UC model and to elucidate the underlying mechanisms involving ferroptosis and the JAK2/STAT3 signaling pathway.
METHODS: A UC model was established by administering 3% DSS in drinking water to male BALB/c mice. Therapeutic efficacy was assessed based on changes in body weight, disease activity index (DAI), colon length, and histopathological alterations. Serum levels of inflammatory cytokines (TNF-α, IL-1β) and oxidative stress markers (MPO, MDA, SOD, GSH) were quantified. Protein expression related to ferroptosis (ACSL4, GPX4), intestinal barrier integrity (Occludin, Claudin-1), and the JAK2/STAT3 pathway was analyzed in colon tissue.
RESULTS: Combined treatment with Ononin and Lactobacillus paracasei significantly alleviated UC symptoms, as shown by improved body weight, colon length, DAI scores, and histopathology. It also reduced pro-inflammatory cytokine levels, suppressed oxidative stress and neutrophil infiltration, and enhanced antioxidant capacity. Mechanistically, the treatment downregulated ACSL4 expression, inhibited JAK2/STAT3 phosphorylation, and upregulated the expression of GPX4, Occludin, and Claudin-1.
CONCLUSION: The combination of Ononin and Lactobacillus paracasei effectively ameliorated DSS-induced colitis in mice. Its protective mechanism involves suppressing inflammation and oxidative stress, inhibiting ferroptosis (potentially through blocking the JAK2/STAT3 pathway), and enhancing intestinal barrier integrity. These findings provide a strong preclinical rationale for developing this combination as a potential therapeutic strategy for UC.
METHODS: A UC model was established by administering 3% DSS in drinking water to male BALB/c mice. Therapeutic efficacy was assessed based on changes in body weight, disease activity index (DAI), colon length, and histopathological alterations. Serum levels of inflammatory cytokines (TNF-α, IL-1β) and oxidative stress markers (MPO, MDA, SOD, GSH) were quantified. Protein expression related to ferroptosis (ACSL4, GPX4), intestinal barrier integrity (Occludin, Claudin-1), and the JAK2/STAT3 pathway was analyzed in colon tissue.
RESULTS: Combined treatment with Ononin and Lactobacillus paracasei significantly alleviated UC symptoms, as shown by improved body weight, colon length, DAI scores, and histopathology. It also reduced pro-inflammatory cytokine levels, suppressed oxidative stress and neutrophil infiltration, and enhanced antioxidant capacity. Mechanistically, the treatment downregulated ACSL4 expression, inhibited JAK2/STAT3 phosphorylation, and upregulated the expression of GPX4, Occludin, and Claudin-1.
CONCLUSION: The combination of Ononin and Lactobacillus paracasei effectively ameliorated DSS-induced colitis in mice. Its protective mechanism involves suppressing inflammation and oxidative stress, inhibiting ferroptosis (potentially through blocking the JAK2/STAT3 pathway), and enhancing intestinal barrier integrity. These findings provide a strong preclinical rationale for developing this combination as a potential therapeutic strategy for UC.