Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common type of liver disease in developed countries. Oxidative stress plays a critical role in the progression of NAFLD. Modern pharmacological study and clinical trials have demonstrated the remarkable antioxidant activity of Gynostemma pentaphyllum (GP) in chronic liver disease. One aim of this study was to explore the potential protective effects and mechanisms of action of GP extract on NAFLD. The in vivo results showed that GP extract could alleviate fatty degeneration and haptic fibrosis in NAFLD mice. For exploring the hepatoprotective mechanisms of GP, we used network pharmacology to predict the potential active components of GP and their intracellular targets in NAFLD. Based on the network pharmacology results, we further utilized biomedical assays to validate this in silico prediction. The results showed that Gypenoside XL could upregulate the protein level of PPARα in NAFLD; the transcription level of several PPARα downstream target genes such as acyl-CoA oxidase (ACO) and carnitine palmitoyltransferase-1 (CPT-1) also increased after Gypenoside XL treatment. The overexpression of ACO and CPT-1 may involve the hepatoprotective effects of GP and Gypenoside XL on NAFLD by regulating mitochondrial fatty acid β-oxidation.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disorder which is related to insulin resistance and metabolic syndrome, such as obesity, diabetes, and hyperlipidemia [1, 2]
Treatments with Gynostemma pentaphyllum (GP) extracts have no obvious effects on the body weight in NAFLD mice (Figure 1(f))
Choline-deficiency amino acid-defined diet (CDAA) diet feeding combined with CCl4 injection significantly induced liver damage in NAFLD mice, as indicated by significant upregulated serum alanine transaminase (ALT) and aspartate transaminase (AST) levels
Summary
Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disorder which is related to insulin resistance and metabolic syndrome, such as obesity, diabetes, and hyperlipidemia [1, 2]. Oxidative stress is one of the key mechanisms responsible for disease progression in NAFLD [3]. Recent studies have shown that fatty acids could induce oxidative stress through regulating the expression or activity of key nuclear receptors such as PPARα, β, γ, liver X receptor (LXRα), retinoid X receptor (RXRα), SREBP-1c, and others [4, 5]. Recent research has demonstrated that GP extracts and its active components may protect alcoholic fatty liver disease in rats through modulating lipid metabolism and reducing oxidative stress. Fuzheng Huayu tablet, a patented Chinese medicine formula from Shanghai Sundise TCM Co., Ltd., has successfully completed Phase II clinical trial in US FDA for treating liver fibrosis in patients with chronic hepatitis C [13, 14].
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