Herbal medicines and nonalcoholic fatty liver disease

Abstract

Nonalcoholic fatty liver disease (NAFLD), which is characterized by excessive fat accumulation in the liver of patients who consume little or no alcohol, becomes increasingly common with rapid economic development. Long-term excess fat accumulation leads to NAFLD and represents a global health problem with no effective therapeutic approach. NAFLD is considered to be a series of complex, multifaceted pathological processes involving oxidative stress, inflammation, apoptosis, and metabolism. Over the past decades, herbal medicines have garnered growing attention as potential therapeutic agents to prevent and treat NAFLD, due to their high efficacy and low risk of side effects. In this review, we evaluate the use of herbal medicines (including traditional Chinese herbal formulas, crude extracts from medicinal plants, and pure natural products) to treat NAFLD. These herbal medicines are natural resources that can inform innovative drug research and the development of treatments for NAFLD in the future.

Keywords: Herbal medicines; Natural product; Nonalcoholic fatty liver disease; Review; Traditional Chinese medicines.

Figure 1

Schematic representation of the pathogenetic mechanism-based nonalcoholic fatty liver disease. NAFLD: Nonalcoholic fatty liver disease; NASH: Nonalcoholic steatohepatitis; FFA: Free fatty acid.

Figure 2

Underlying mechanisms of herbal medicines for the treatment of nonalcoholic fatty liver disease. Medicines may prevent cellular damage in hepatocytes associated with NAFLD through different mechanism of action including: (1) depressing lipogenesis through down-regulating sterol regulatory element-binding protein 1c (SREBP-1c); (2) increasing β-fatty acid (FA) oxidation by up-regulating peroxisome proliferator activated receptor α (PPARα); (3) increasing insulin sensitivity and depressing oxidative stress through increased antioxidant levels via nuclear factor-erythroid 2-related factor 2 (Nrf2); and (4) inhibiting activation of inflammatory pathways. TNFR: TNFα receptor; IL6-R: IL-6 receptor; IR: Insulin receptor; CD36: Cluster of differentiation 36/FA translocase; p-AMPK: Phosphorylated AMP-activated protein kinase α; ACC: Acetyl-CoA carboxylase; FAS: Fatty acid synthase; SCD: Stearoyl-CoA desaturase; GPAT: Glycerol-3-phosphate acyltransferase; CPT-1: Carnitine palmitoyl transferase 1; ACO: Acyl-CoA oxidase; PGC-1: PGC1α: PPARγ coactivator-1α; JNK: c-Jun N-terminal kinase; PKC: Protein kinase C; mTOR: Mammalian target of rapamycin.

Figure 3

Chemical structures of flavonoids and polyphenols for the treatment of nonalcoholic fatty liver disease.

Figure 4

Chemical structures of other kinds of pure natural products for the treatment of nonalcoholic fatty liver disease.