关键词: Fam172a, 细胞外调节蛋白激酶, 脂毒性, 非酒精性脂肪肝

Abstract: Objective To preliminarily explore the mechanism of Fam172a gene knockout in lipid toxic liver cell injury. Methods Fam172a gene knockout (Fam172a - / - ) mice was used to assess liver function, liver tissue lipid accumulation, and inflammatory cytokine levels. Fam172a geneknockdown HepG2 cell lines were performed to assess intracellular lipid accumulation and inflammato
ry cytokine levels. Protein levels were analyzed via Western blotting. Results Compared to the controlgroup, Fam172a - / - mice exhibited significantly elevated serum ALT and AST levels, aggravated hepatic structural damage, lipid accumulation, and inflammation. Moreover, there was a significant upregulation in hepatic pERK/ ERK relative expression levels. Fam172a gene knockdown led to increased triglyceride content and inflammatory cytokine levels in HepG2 cells, along with a significant elevation in the relative expression level of pERK/ ERK. However, the administration of the ERK inhibitor U0126 notably mitigated the lipotoxic hepatocyte injury induced by Fam172a gene knockdown. Conclusion Fam172a gene knockdown exacerbates hepatocyte lipotoxicity through the activation of the ERK pathway.

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