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. 2022 May 11;2022:9233650. doi: 10.1155/2022/9233650

Figure 3.

Figure 3

Molecular mechanisms of antioxidant-mediated nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) regression. SIL: silymarin; SBN: silibinin/silybin; VA: vitamin A; VC: vitamin C; VE: vitamin E; RES: resveratrol; PTX: pentoxifylline; LPO: lipid peroxidation; FFA: free fatty acids; DNL: de novo lipogenesis; DGAT: diglyceride acyltransferase; LD: lipid droplets; M: mitochondria; N: nucleus; ETC: electron transport chain; PPAR-α: peroxisome proliferator-activated receptor-alpha; TG: triglyceride; IR: insulin resistance; SREBP1c: sterol regulatory element-binding transcription factor 1c; ACC: acetyl-CoA carboxylase; FAS: fatty acid synthase; SCDs: stearoyl-CoA desaturase; DAGs: diacylglycerols; ER: endoplasmic reticulum; qHSCs: quiescent hepatic stellate cells; ILs: interleukins; TNF-α: tumor necrosis factor-α; NF-κB: nuclear factor-kappa B; TGF-β: transforming growth factor-β; ECM: extracellular matrix; OS: oxidative stress; Meth: methylation; NRF-2: nuclear factor erythroid 2-related factor 2; ARE: antioxidant response element; UPR: unfolded protein response; PERK: PKR-like ER kinase; AMPK: 5′ AMP-activated protein kinase; GRP78: glucose-regulated protein 78; eIF2α: phosphorylation of eukaryotic initiation factor-2α; ATF 4 and 6: activating transcription factor 4 and 6; IRE1: inositol-requiring enzyme 1; CHOP: CCAAT-enhancer-binding protein homologous protein; ROS: reactive oxygen species; JNK: c-Jun N-terminal kinase.