Truncated thrombospondin-1 polypeptide alleviates non-alcoholic fatty liver disease induced by palmitic acid and high-fat diets

  • Int J Biol Macromol. 2025 Oct 17;331(Pt 1):148308. doi: 10.1016/j.ijbiomac.2025.148308.
Keke Zhang  1 ,  Shiqi Li  1 ,  Xiaocan Sun  1 ,  Hongkun Ma  2 ,  Ying Li  3 ,  Yu Pan  1 ,  Jingruo Liu  1 ,  Xianru Geng  1 ,  Yingchao Wan  1 ,  Dan Wu  4
Affiliations
  • 1. Heilongjiang Province Key Laboratory of Anti-fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, Heilongjiang, China; College of Life Sciences, Mudanjiang Medical University, Mudanjiang, Heilongjiang, China.
  • 2. Public Health College, Mudanjiang Medical University, Mudanjiang, China; Key Laboratory of Chronic Disease Etiology and Prevention and Treatment of Border Region in Heilongjiang, Mudanjiang Medical University, Mudanjiang, China.
  • 3. Key Laboratory of Chronic Disease Etiology and Prevention and Treatment of Border Region in Heilongjiang, Mudanjiang Medical University, Mudanjiang, China; Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Heilongjiang, China.
  • 4. Heilongjiang Province Key Laboratory of Anti-fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, Heilongjiang, China; College of Life Sciences, Mudanjiang Medical University, Mudanjiang, Heilongjiang, China. Electronic address: [email protected].
PMID: 41109376 DOI: 10.1016/j.ijbiomac.2025.148308
Abstract

Non-alcoholic fatty liver disease (NAFLD) is a metabolic stress-induced liver injury. Thrombospondin-1 (Thbs-1) is associated with NAFLD and has the potential to reduce lipid accumulation in hepatocytes. The aim of the study was to construct and screen truncated Thbs-1 polypeptide, and to investigate the function in palmitic acid (PA)-induced AML12 cells and High-fat diet (HFD)-induced C57BL/6 mice. The recombinant truncated Thbs-1 plasmids were constructed and the polypeptides were purified. The effects of the polypeptides were investigated in PA-induced AML12 cells and HFD-induced mice to screen the target polypeptide. The results showed that TSRC could alleviate the histopathological changes of NAFLD mice, reduce the expression of inflammatory factors and lipid metabolism-related factors. In conclusion, TSRC could ameliorate inflammation and lipid accumulation in PA-induced AML12 cells, relieve liver pathological changes, improve liver function, and effectively alleviate NAFLD in HFD-induced C57BL/6 mice.

Keywords
Lipid metabolism; NAFLD; Thbs-1.
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