Abstract
Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease with high prevalence in the developed countries. NAFLD has been considered as one of the leading causes of cryptogenic cirrhosis and chronic liver disease. The individuals with obesity, insulin resistance and diabetes mellitus, hyperlipidaemia, and hypertension cardiovascular disease have a high risk to develop NAFLD. The related critical pathological events are associated with the development of NAFLD including insulin resistance, lipid metabolism dysfunction, oxidative stress, inflammation, apoptosis, and fibrosis. The development of NAFLD range from simple steatosis to non-alcoholic steatohepatitis (NASH). Hepatic steatosis is characterized by fat accumulation, which represents the early stage of NAFLD. Then, inflammation triggered by steatosis drives early NAFLD progression into NASH. Therefore, the amelioration of steatosis and inflammation is essential for NAFLD therapy. The herbal medicine have taken great effects on the improvement of steatosis and inflammation for treating NAFLD. It has been found out that these effects involved the multiple mechanisms underlying lipid metabolism and inflammation. In this review, we pay particular attention on herbal medicine treatment and make summary about the research of herbal medicine, including herb formula, herb extract and naturals compound on NAFLD. We make details about their protective effects, the mechanism of action involved in the amelioration steatosis and inflammation for NAFLD therapy as well as the clinical application.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease, and it is associated high metabolic risk of health problem such as dyslipidemia, insulin resistance, obesity and type II diabetic disease
AMPK action activated by herbal medicine involves in de novo lipid synthesis associated with the suppression of SREBP-1c, Fatty Acid Synthase (FAS), Acetyl-CoA Carboxylase (ACC), and SCD-1expression, and increase b-oxidation defense that improves hepatic fatty acids efflux via the modulation of Carnitine Palmitoyltransferase-1 (CPT-1) and PPARa production
These have been supported by the evidence that total aralosides from aralia elata (Miq) seem protected mice against HFDinduced cellular apoptosis, as suggested by TUNEL staining, and ameliorated non-alcoholic steatohepatitis (NASH) by inhibiting the nuclear factor-kB (NF-kB)/IRE1a/JNK/ IkB activation in ApoE-/- mice (Luo et al, 2015); Lycium barbarum polysaccharides partially modulated hepatocyte apoptosis process via NF-kB/mitogen-activated protein kinases (MAPKs) pathways, which has been proved to be related to the biological activity of l-arabinose and b-carotene in polysaccharides (Xiao et al, 2014)
Summary
Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease, and it is associated high metabolic risk of health problem such as dyslipidemia, insulin resistance, obesity and type II diabetic disease. Non-Alcoholic Steatohepatitis (NASH), a severer form characterized by fat build-up, varying degrees of inflammation and ballooning degeneration of liver cells could be developed. The antioxidant reagent such as Vitamin E has been suggested to treat non-diabetic patients with NASH as evidenced by a recent clinical trial (Sanyal et al, 2010); The use of lipid-lowering agents such as statin has been shown to reduce the risk of mortality or liver transplant in NAFLD patients (German et al, 2019); As sodium-glucose cotransporter 2 (SGLT2) inhibitors, Dapagliflozin and Canagliflozin could decrease hepatic lipid accumulation and significantly improve liver function (Arase et al, 2019). Progress in drug development of NAFLD has been found major advances with herbal medicines which are regarded as abundant sources of natural bioactive chemicals that improve hepatic functions. We have provided an overview of herbal medicine (including herbal formula, crude extract, and pure bioactive compound form medicinal plants) approaches which have demonstrated their ability to counteract NAFLD in human patients and animal models
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