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    Home > Active Ingredient News > Digestive System Information > Hepatology: Lebinin 22 can improve inflammation of non-alcoholic fatty hepatitis, which is driven by neophilic granulocytes.

    Hepatology: Lebinin 22 can improve inflammation of non-alcoholic fatty hepatitis, which is driven by neophilic granulocytes.

    • Last Update: 2020-09-19
    • Source: Internet
    • Author: User
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    Background and target non-alcoholic fatty liver diseases include a range of diseases such as simple fatty degeneration, non-alcoholic fatty hepatitis (NASH), cirrhosis and liver cancer.
    , how simple fat degeneration develops into NASH remains unclear and there is a lack of effective therapies.
    C-X-C base sequence degeneration factor ligation 1 (CXCL1) was a key degeneration factor for neutral granulocyte immersion, with significant increases in expression in NASH patients, but not in obese individuals or mice on a high-fat diet (HFD).
    the purpose of this study was to test whether overexploitation of CXCL1 itself in the liver induced NASH in MICEH-fed mice, and to test the therapeutic effectiveness of IL-22 in this NASH disease.
    method and results the researchers promoted fat degeneration to NASH progression in MICEH in mice fed HFD by inducing neutrophil immersion, oxidative stress, and kinase activity in mice over-expressed by CXCL1.
    Neutrophil Cytogenetic Factor 1 (Ncf1)/p47 phox myelin-specific absence of this gene-coded NADPH oxidase 2 complex, which significantly reduced THESH and stress kinase activation induced by CXCL1 in mice fed HFD.
    leucin (IL)-22 can improve the level of NASH inflammation induced by CXCL1 / HFD or methionine-choline deficiency diet-induced.
    addition, although IL-22 does not target immune cells, it weakens the inflammatory function of the extracellular vesicles derived from liver cells rich in mitochondrial DNA, thereby inhibiting inflammation of the liver in NASH.
    Conclusion This study confirms that excessive expression of CXCL1 in the liver can lead to liver fat degeneration in HDD-fed mice through the activation of neutrophil-derived reactive oxygen and stress kinases, but this can be reversed by IL-22 therapy that induces metal sulfur protein.
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