Hepatocyte steatosis activates macrophage inflammatory response accelerating atherosclerosis development.

ABSTRACT:

Objectives

To investigate the mechanism of comorbidity between non-alcoholic fatty liver disease (NAFLD) and atherosclerosis (AS) based on metabolomics and network pharmacology.

Methods

Six ApoE^－/－ mice were fed with a high-fat diet for 16 weeks as a comorbid model of NAFLD and AS (model group). Normal diet was given to 6 wildtype C57BL/6J mice (control group). Serum samples were taken from both groups for a non-targeted metabolomics assay to identify differential metabolites. Network pharmacology was applied to explore the possible mechanistic effects of differential metabolites on AS and NAFLD. An in vitro comorbid cell model was constructed using NCTC1469 cells and RAW264.7 macrophage. Cellular lipid accumulation, cell viability, morphology and function

SUBMITTER: Li Y 

PROVIDER: S-EPMC10764189 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature