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<p>Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by recurrent inflammation and mucosal damage. Loganin, a natural iridoid glycoside with anti-inflammatory and antioxidant properties, has shown protective effects in experimental colitis. However, its role in regulating mitochondrial dysfunction, oxidative stress-induced epithelial cell apoptosis, and barrier injury in UC remains incompletely understood. A dextran sulfate sodium (DSS)-induced colitis model was established in mice, and an H<sub>2</sub>O<sub>2</sub>-induced epithelial injury model was established in Caco-2 cells to evaluate the protective effects of loganin in vivo and in vitro. Colonic injury, oxidative stress, apoptosis, and barrier integrity were assessed by histological analysis, biochemical assays, immunofluorescence, Western blotting, flow cytometry, TEER measurement, and FITC-dextran permeability analysis. Mitochondrial dysfunction was evaluated by measuring mitochondrial membrane potential, mtROS accumulation, cytochrome c redistribution, and mitochondrial ultrastructure. In addition, network pharmacology, molecular docking, and IL-6 supplementation experiments were performed to explore the involvement of IL-6/STAT3/Bcl-2-related signaling in the anti-apoptotic effects of loganin. Loganin significantly alleviated histological damage and preserved colonic architecture in DSS-treated mice. It reduced oxidative stress, as evidenced by lower MDA levels, enhanced antioxidant enzyme activity, and improved intestinal barrier function. Loganin treatment also suppressed epithelial cell apoptosis, as shown by decreased BAX and cleaved caspase-3 levels and increased Bcl-2 expression. In H<sub>2</sub>O<sub>2</sub>-injured Caco-2 cells, loganin attenuated mitochondrial dysfunction, preserved mitochondrial membrane potential, and reduced mtROS intensity from 16.54% to 10.11%. Loganin also reduced the apoptosis rate from 29.05% to 12.68% and improved epithelial integrity. These findings support the involvement of IL-6/STAT3/Bcl-2-related signaling in the protective effects of loganin. Our findings suggest that loganin alleviates oxidative stress-induced epithelial cell apoptosis and mitochondrial dysfunction in experimental colitis models. These protective effects are associated with modulation of IL-6/STAT3/Bcl-2-related signaling. Collectively, this study extends previous evidence on the protective effects of loganin in colitis and provides additional mechanistic insight into its role in epithelial homeostasis and barrier integrity.</p>

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Loganin alleviates oxidative stress-induced apoptosis by modulating mitochondrial function and STAT3 signaling in DSS-induced colitis and H2O2-injured Caco-2 cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月28日

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  • Guofeng Li,
  • Shuai Zhou,
  • Xing Zhao,
  • Yongfeng Cheng,
  • Zhihua Ma

摘要

Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by recurrent inflammation and mucosal damage. Loganin, a natural iridoid glycoside with anti-inflammatory and antioxidant properties, has shown protective effects in experimental colitis. However, its role in regulating mitochondrial dysfunction, oxidative stress-induced epithelial cell apoptosis, and barrier injury in UC remains incompletely understood. A dextran sulfate sodium (DSS)-induced colitis model was established in mice, and an H2O2-induced epithelial injury model was established in Caco-2 cells to evaluate the protective effects of loganin in vivo and in vitro. Colonic injury, oxidative stress, apoptosis, and barrier integrity were assessed by histological analysis, biochemical assays, immunofluorescence, Western blotting, flow cytometry, TEER measurement, and FITC-dextran permeability analysis. Mitochondrial dysfunction was evaluated by measuring mitochondrial membrane potential, mtROS accumulation, cytochrome c redistribution, and mitochondrial ultrastructure. In addition, network pharmacology, molecular docking, and IL-6 supplementation experiments were performed to explore the involvement of IL-6/STAT3/Bcl-2-related signaling in the anti-apoptotic effects of loganin. Loganin significantly alleviated histological damage and preserved colonic architecture in DSS-treated mice. It reduced oxidative stress, as evidenced by lower MDA levels, enhanced antioxidant enzyme activity, and improved intestinal barrier function. Loganin treatment also suppressed epithelial cell apoptosis, as shown by decreased BAX and cleaved caspase-3 levels and increased Bcl-2 expression. In H2O2-injured Caco-2 cells, loganin attenuated mitochondrial dysfunction, preserved mitochondrial membrane potential, and reduced mtROS intensity from 16.54% to 10.11%. Loganin also reduced the apoptosis rate from 29.05% to 12.68% and improved epithelial integrity. These findings support the involvement of IL-6/STAT3/Bcl-2-related signaling in the protective effects of loganin. Our findings suggest that loganin alleviates oxidative stress-induced epithelial cell apoptosis and mitochondrial dysfunction in experimental colitis models. These protective effects are associated with modulation of IL-6/STAT3/Bcl-2-related signaling. Collectively, this study extends previous evidence on the protective effects of loganin in colitis and provides additional mechanistic insight into its role in epithelial homeostasis and barrier integrity.