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<p>LC2767, a mix of <i>Lactiplantibacillus plantarum</i> LC27 and <i>Bifidobacterium longum</i> LC67, alleviates high-fat diet- or alcohol-induced liver injury and steatosis in mice. In the present study, we examined the action mechanism of LC2767 on lipopolysaccharide (LPS)-, LPS/D-galactosamine (LGc)-, or LPS/thioacetamide (LTc)-induced liver damage and fibrosis in mice. Short-termly or long-termly intraperitoneal injection of LPS, LGc, or LTc caused liver damage and fibrosis in mice: they increased alanine transaminase (ALT), aspartate transaminase (AST), and γ-glutamyl transpeptidase (γ-GTP) in the blood and α-smooth muscle actin (SMA) and tumor necrosis factor (TNF)-α expression and NF-κB activation in the liver. Short-termly orally gavage of LPS also caused liver damage. However, oral administration of LC2767 significantly reduced LPS- or LGc-, or LTc-induced ALT, AST, and γ-GTP levels in the blood. LC2767 also suppressed LPS- or LGc-induced collagen-1, α-SMA, TNF-α, CYP7A1, tissue inhibitor of metalloproteinase (TIMP)-1, and matrix metalloproteinase (MMP)-14 expression, NF-κB activation, non-alcoholic fatty liver disease activity score, and fibrosis score in the liver, and TNF-α expression and NF-κB activation in the colon, while LPS- or LGc-suppressed farnesoid X receptor (FXR) expression was increased in the liver and colon. Furthermore, LC2767 alleviated LPS-induced gut dysbiosis: it increased <i>Akkermansiaceae</i> population and decreased LPS-producing <i>Christensenellaceae</i>,<i> Porphyromonadaceae</i>, and <i>Rhodospirillaceae</i> populations. These findings suggest that LC2767 can alleviate liver damage and fibrosis by regulating NF-κB activation, FXR expression, and gut microbiota.</p>

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LC2767 alleviates LPS-induced liver injury and fibrosis by regulating FXR expression, NF-κB activation, and gut microbiota

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月6日

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  • Dong-Yun Lee,
  • Hyo-Min Jang,
  • Jung-Woo Shin,
  • Yoon-Jung Shin,
  • Sung Hye Kim,
  • Seung-Won Han,
  • Dong-Hyun Kim

摘要

LC2767, a mix of Lactiplantibacillus plantarum LC27 and Bifidobacterium longum LC67, alleviates high-fat diet- or alcohol-induced liver injury and steatosis in mice. In the present study, we examined the action mechanism of LC2767 on lipopolysaccharide (LPS)-, LPS/D-galactosamine (LGc)-, or LPS/thioacetamide (LTc)-induced liver damage and fibrosis in mice. Short-termly or long-termly intraperitoneal injection of LPS, LGc, or LTc caused liver damage and fibrosis in mice: they increased alanine transaminase (ALT), aspartate transaminase (AST), and γ-glutamyl transpeptidase (γ-GTP) in the blood and α-smooth muscle actin (SMA) and tumor necrosis factor (TNF)-α expression and NF-κB activation in the liver. Short-termly orally gavage of LPS also caused liver damage. However, oral administration of LC2767 significantly reduced LPS- or LGc-, or LTc-induced ALT, AST, and γ-GTP levels in the blood. LC2767 also suppressed LPS- or LGc-induced collagen-1, α-SMA, TNF-α, CYP7A1, tissue inhibitor of metalloproteinase (TIMP)-1, and matrix metalloproteinase (MMP)-14 expression, NF-κB activation, non-alcoholic fatty liver disease activity score, and fibrosis score in the liver, and TNF-α expression and NF-κB activation in the colon, while LPS- or LGc-suppressed farnesoid X receptor (FXR) expression was increased in the liver and colon. Furthermore, LC2767 alleviated LPS-induced gut dysbiosis: it increased Akkermansiaceae population and decreased LPS-producing Christensenellaceae, Porphyromonadaceae, and Rhodospirillaceae populations. These findings suggest that LC2767 can alleviate liver damage and fibrosis by regulating NF-κB activation, FXR expression, and gut microbiota.