Plant-Based Foods and Their Bioactive Compounds on Fatty Liver Disease: Effects, Mechanisms, and Clinical Application

Figure 2

The molecular mechanisms of plant-based foods in the alleviation of NAFLD. The major molecular mechanisms include the alleviation of hepatic steatosis, oxidative stress, inflammation, gut dysbiosis, and the regulation of autophagy. To be specific, fruits, spices, and teas alleviated hepatic steatosis by activating AMPK, PPAR-α, SIRT1, and FXR and inhibiting PPAR-γ pathways. Besides, the antioxidative stress property of such plants was mainly associated with the activation of the Nrf2 pathway. Moreover, plant-based foods could alleviate inflammation by activating SIRT1, while inhibiting NF-κB pathways. Furthermore, these plants alleviated gut dysbiosis by regulating the abundance of Akkermansia, Bacteroides, Firmicutes, and Lactobacillus. Also, such plants could regulate autophagy by inhibiting the Akt pathway and reducing the production of autophagic biomarkers. Akt: protein kinase B; AMPK: adenosine 5-monophosphate-activated protein kinase; ARE: Nrf2-antioxidant response element; CYP2E1: cytochrome P450 2E1; FAS: fatty acid synthase; FXR: farnesoid X receptor; IL-1β/6/8: interleukin-1β/6/8; LXRα: liver X receptor α; mTOR: mammalian target rapamycin; NF-κB: nuclear factor kappa-B; Nrf2: nuclear factor erythroid 2-related factor 2; PGC-1α: peroxisomal proliferator-activated receptor-gamma coactivator-1α; PKA: protein kinase A; PPAR-α/γ: peroxisome proliferator-activated receptor-α/γ; ROS: reactive oxygen species; SIRT1: sirtuin 1; SOD: superoxide dismutase; SREBP-1c: sterol regulatory element-binding transcription factor 1c; TNF-α: tumor necrosis factor-α.