Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease characterized by excessive fat accumulation in the liver. The aim of this study is to elucidate the multi-target mechanism of polyphenols in blueberry leaves (PBL) on NAFLD by network pharmacology and to validate its results via biological experiments. Twenty constituents in PBL were preliminarily determined by liquid chromatography-tandem mass spectrometry. Subsequently, 141 predicted drug targets and 1226 targets associated with NAFLD were retrieved from public databases, respectively. The herb-compound-target network and the target protein–protein interaction network (PPI) were established through Cytoscape software, and four compounds and 53 corresponding targets were identified. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were performed to explore the biological processes of the predicted genes. The results of cell experiments demonstrated that PBL could significantly improve the viability of the NAFLD cell model, and the protein expressions of caspase-3 and Bcl-2 were consistent with the expected mechanism of action of PBL. Those results systematically revealed that the multi-target mechanism of PBL against NAFLD was related to the apoptosis pathway, which could bring deeper reflections into the hepatoprotective effect of PBL.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is regarded as the most common cause of liver disease in many developed countries, and its incidence is increasing dramatically in developing countries [1,2]
53 key target genes for polyphenols in blueberry leaves (PBL) in the treatment of NAFLD were obtained based on the Venn diagram
According to the apoptosis results, PBL could effectively alleviate the early apoptosis of NAFLD-modeled cells and increase the proportion of living cells
Summary
Non-alcoholic fatty liver disease (NAFLD) is regarded as the most common cause of liver disease in many developed countries, and its incidence is increasing dramatically in developing countries [1,2]. It is characterized by steatosis, inflammation, hepatocellular ballooning, hepatocellular injury, etc., which may progress to non-alcoholic steatohepatitis (NASH), and even induce the development of liver cirrhosis or hepatocellular carcinoma [3,4,5]. Junli Zhang et al [11] reported that baicalin (BA) significantly inhibited hepatocyte apoptosis in methionine and choline-deficient (MCD) diet-induced mice by reducing apoptotic cells and the protein level of caspases-3.
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