Herbal medicines and nonalcoholic fatty liver disease

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.