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<p>Ulcerative colitis (UC) is a chronic inflammatory disorder characterized by recurrent and intermittent episodes of inflammation. (-)-Myrtenol (MYR) has been shown to exhibit anti-inflammatory, antioxidant, and gastroprotective properties; however, its therapeutic potential in UC remains unexplored. In this study, we established in vitro UC models using lipopolysaccharide (LPS)-induced Caco-2 cells and in vivo models using dextran sulfate sodium (DSS)-induced mice to investigate the effects of MYR on UC. Our findings demonstrated that MYR protected Caco-2 cells from LPS-induced apoptosis and restored mitochondrial function by activating mitophagy. Mechanistically, MYR exerted its protective effects by upregulating ANXA1 expression in LPS-challenged Caco-2 cells, which subsequently activated the PINK1/Parkin pathway. Consistent with these in vitro results, experiments in the DSS-induced mouse model revealed that MYR alleviated UC symptoms and mitigated mitochondrial damage through the regulation of the ANXA1/PINK1/Parkin pathway-mediated mitophagy. In conclusion, MYR reduced apoptosis in LPS-induced Caco-2 cells and ameliorated UC symptoms in DSS-induced mice by enhancing mitophagy and alleviating mitochondrial dysfunction via the ANXA1/PINK1/Parkin pathway.</p>

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Myrtenol ameliorates ulcerative colitis by modulating ANXA1/PINK1/Parkin-mediated mitophagy

  • 期刊论文

  • 发表日期：

    2025年7月31日

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  • Yimin Li,
  • Xiaobing Gong,
  • Yinghua Peng,
  • Yadang Kuang,
  • Jiaxuan Huang,
  • Mengli Zheng,
  • Leilei Zhan,
  • Jiewen Liang,
  • Weiyi Guo

摘要

Ulcerative colitis (UC) is a chronic inflammatory disorder characterized by recurrent and intermittent episodes of inflammation. (-)-Myrtenol (MYR) has been shown to exhibit anti-inflammatory, antioxidant, and gastroprotective properties; however, its therapeutic potential in UC remains unexplored. In this study, we established in vitro UC models using lipopolysaccharide (LPS)-induced Caco-2 cells and in vivo models using dextran sulfate sodium (DSS)-induced mice to investigate the effects of MYR on UC. Our findings demonstrated that MYR protected Caco-2 cells from LPS-induced apoptosis and restored mitochondrial function by activating mitophagy. Mechanistically, MYR exerted its protective effects by upregulating ANXA1 expression in LPS-challenged Caco-2 cells, which subsequently activated the PINK1/Parkin pathway. Consistent with these in vitro results, experiments in the DSS-induced mouse model revealed that MYR alleviated UC symptoms and mitigated mitochondrial damage through the regulation of the ANXA1/PINK1/Parkin pathway-mediated mitophagy. In conclusion, MYR reduced apoptosis in LPS-induced Caco-2 cells and ameliorated UC symptoms in DSS-induced mice by enhancing mitophagy and alleviating mitochondrial dysfunction via the ANXA1/PINK1/Parkin pathway.