Abstract
Pure total flavonoids from Citrus (PTFC) effectively reduce the symptoms of non-alcoholic fatty liver disease (NAFLD). Our previous microarray analysis uncovered the alterations of important signaling pathways in the treatment of NAFLD with PTFC. However, the underlying core genes that might be targeted by PTFC, which play important roles in the progression of NALFD are yet to be identified. In this study, we predicted the vascular endothelial growth factor-C (VEGF-C) as potential key molecular target of PTFC against NAFLD via network pharmacology analysis. The network pharmacology approach presented here provided important clues for understanding the mechanisms of PTFC treatment in the development of NAFLD.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is rapidly becoming a major healthcare problem worldwide affecting 15–30% population in Asia (Srivastava et al, 2017)
We previously found that pure total flavonoids from Citrus (PTFC) attenuated non-alcoholic steatohepatitis (NASH) symptoms
Comparing the above two networks, we found two common hub genes vascular endothelial growth factor-C (VEGF-C) and COL4A1 which occurred in both networks of NAFLD progression and Pure total flavonoids from Citrus (PTFC) treatment groups
Summary
Non-alcoholic fatty liver disease (NAFLD) is rapidly becoming a major healthcare problem worldwide affecting 15–30% population in Asia (Srivastava et al, 2017). It is defined as abnormal hepatic lipid accumulation (>5% by weight) without excessive alcohol intake (Nalbantoglu and Brunt, 2014). NAFLD is considered to be a hepatic manifestation of metabolic syndrome (Takahashi et al, 2015), which is closely associated with obesity, insulin resistance, diabetes and hypertriglyceridemia (Kirpich et al, 2011). NAFLD may progress from simple steatosis (SS) into a more severe form, non-alcoholic steatohepatitis (NASH) (Konerman et al, 2017). NASH has become the third most common indication for liver transplantation in the United States (Takahashi et al, 2015)
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