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

Figure 3

The molecular mechanisms of plant-based foods in the alleviation of AFLD. The major molecular mechanisms include the promotion of ethanol metabolism and inhibition of apoptosis, hepatic steatosis, oxidative stress, inflammation, and gut dysbiosis. First of all, plant-based foods accelerated ethanol metabolism by increasing the activities of ALD and ALDH. Also, these plants inhibited apoptosis by activating the SIRT1 pathway. Moreover, they could alleviate hepatic steatosis by activating the AMPK-PPAR-α pathway and regulating lipid homeostasis-related genes (like HNF4A and PTP1B). Furthermore, the antioxidative effect of such plants was related to the upregulation of the Nrf2 pathway. Besides, edible plants ameliorated inflammation by inhibiting TLR4 and NF-κB pathways. Additionally, these plants attenuated gut dysbiosis by regulating the abundance of Bacteroides and Firmicutes. AMPK: adenosine 5-monophosphate-activated protein kinase; ARE: Nrf2-antioxidant response element; CPT-1: carnitine palmitoyltransferase 1; CYP2E1: cytochrome P450 2E1; FAS: fatty acid synthase; IL-1β/6/8: interleukin-1β/6/8; NF-κB: nuclear factor kappa-B; Nrf2: nuclear factor erythroid 2-related factor 2; PPAR-α: peroxisome proliferator-activated receptor-α; ROS: reactive oxygen species; SOD: superoxide dismutase; SREBP-1c: sterol regulatory element-binding transcription factor 1c; TNF-α: tumor necrosis factor-α.