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<p>This study elucidates the anti-colorectal cancer (CRC) mechanism of <i>Rosa rugosa</i> cv. Plena polysaccharide RPP1 against AOM/DSS-induced carcinogenesis. Purified via water extraction and chromatography, RPP1 was characterized as an eight-monosaccharide polymer by HPLC. In CRC mice, RPP1 administration reduced colonic polyp formation and ameliorated colon shortening while normalizing elevated serum IL-1β and TNF-α levels. Integrated multi-omics analyses revealed RPP1 remodeled gut microbiota composition through suppression of pro-inflammatory <i>Bacteroides</i> and <i>Desulfovibrio</i> concurrent with enrichment of beneficial <i>Eubacterium</i> and <i>Muribaculum</i>. These microbial shifts were associated with downregulation of fecal phosphatidylcholine (PC) and lysophosphatidylcholine (LPC), perturbing ether lipid, glycerophospholipid and sphingolipid metabolism. Mechanism correlation analysis further indicated <i>Muribaculum</i>/<i>Clostridium</i> modulation mediated RPP1’s regulation of LPC levels. Transcriptomics confirmed suppression of lipid-metabolism pathways alongside activation of NOD-like receptor (NLR) and PPAR immune signaling. Collectively, RPP1 alleviates CRC through multifaceted modulation of gut microbiota, lipidomic remodeling, and immune pathway activation.</p>

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Polysaccharides derived from Rosa rugosa cv. Plena ameliorate colorectal cancer by regulating intestinal microbiota composition and lipid metabolism pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月14日

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  • Chunyu Dai,
  • Xuan Zheng,
  • Jingxin Zhu,
  • Hongxing Zhang,
  • Junhua Jin,
  • Xiaona Pang,
  • Xiangyang Li,
  • Yuanhong Xie

摘要

This study elucidates the anti-colorectal cancer (CRC) mechanism of Rosa rugosa cv. Plena polysaccharide RPP1 against AOM/DSS-induced carcinogenesis. Purified via water extraction and chromatography, RPP1 was characterized as an eight-monosaccharide polymer by HPLC. In CRC mice, RPP1 administration reduced colonic polyp formation and ameliorated colon shortening while normalizing elevated serum IL-1β and TNF-α levels. Integrated multi-omics analyses revealed RPP1 remodeled gut microbiota composition through suppression of pro-inflammatory Bacteroides and Desulfovibrio concurrent with enrichment of beneficial Eubacterium and Muribaculum. These microbial shifts were associated with downregulation of fecal phosphatidylcholine (PC) and lysophosphatidylcholine (LPC), perturbing ether lipid, glycerophospholipid and sphingolipid metabolism. Mechanism correlation analysis further indicated Muribaculum/Clostridium modulation mediated RPP1’s regulation of LPC levels. Transcriptomics confirmed suppression of lipid-metabolism pathways alongside activation of NOD-like receptor (NLR) and PPAR immune signaling. Collectively, RPP1 alleviates CRC through multifaceted modulation of gut microbiota, lipidomic remodeling, and immune pathway activation.