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CN 22-1108/R
Volume 40 Issue 1
Jan.  2024
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Article Navigation >  Journal of Clinical Hepatology  > 2024  >  40(1): 64-69

Role of salidroside in a mouse model of non-alcoholic fatty liver disease： A study based on nicotinamide phosphoribosyltransferase

DOI: 10.12449/JCH240112
  • 1.

    Department of Spleen，Stomach and Liver Diseases，Luzhou Hospital of Traditional Chinese Medicine，Luzhou，Sichuan 646000，China

  • 2.

    Department of General Practice，The Affiliated Hospital of Southwest Medical University，Luzhou，Sichuan 646000，China

Research funding:

Southwest Medical University-Luzhou Traditional Chinese Medicine Hospital Base Project (2017-LH012)

  • Received Date: 2023-04-09
  • Accepted Date: 2023-05-26
  • Published Date: 2024-01-23
    Abstract
  •   Objective  To investigate the protective effect of salidroside against nonalcoholic fatty liver disease （NAFLD） and its mechanism of action.  Methods  A total of 24 male KM mice were randomly divided into normal group， HFD group， HFD+blank control group， and HFD+salidroside group， with 6 mice in each group. The mice in the normal group were given normal diet， and those in the other groups were given high-fat diet. After 14 weeks of modeling， the mice were given salidroside 100 mg/kg/day by gavage， and related samples were collected at the end of week 22. Enzyme-linked immunosorbent assay was used to measure the serum levels of related biochemical parameters including alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， triglyceride （TG）， total cholesterol （TC）， high-density lipoprotein cholesterol （HDL-C）， and low-density lipoprotein cholesterol （LDL-C）； HE staining and NAFLD activity score （NAS） were used to observe the liver histopathology of mice； Western blot was used to measure the changes in the expression of NAMPT， Sirt1， AMPKα， and SREBP1 in liver tissue. A one-way analysis of variance was used for comparison between multiple groups， and the least significant difference t-test was used for further comparison between two groups.  Results  Compared with the normal group， the HFD group had obvious steatosis and extensive large lipid droplets in liver tissue， with significant increases in NAS score （P<0.01） and the content of AST， ALT， TG， TC， and LDL-C in peripheral blood （all P<0.05） and a significant reduction in the content of HDL-C （P<0.05）， as well as significant reductions in the expression levels of NAMPT， AMPKα， and Sirt1 in liver tissue （all P<0.05） and a significant increase in the expression level of SERBP1 （P<0.01）. Compared with the HFD group and the HFD+blank control group， the HFD+salidroside group had reductions in the distribution of vacuolar lipid droplets and intralobular inflammation in liver tissue， alleviation of the ballooning degeneration of hepatocytes， significant reductions in NAS score （P<0.01） and the content of AST， ALT， TG， and LDL-C in peripheral blood （all P<0.05）， and a significant increase in the content of HDL-C （P<0.05）， as well as significant increases in the expression levels of NAMPT， AMPKα， and Sirt1 in liver tissue （all P<0.05） and a significant reduction in the expression level of SERBP1 （P<0.01）.  Conclusion  Salidroside can significantly improve the pathological state of mice with NAFLD induced by high-fat diet and exert a protective effect against NAFLD by increasing the expression of NAMPT， Sirt1， and AMPKα and reducing the expression of SERBP1.

     

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