Figure 1.

An overview of the pathophysiological mechanisms that oxidative stress and inflammation in the development of non-alcoholic fatty liver disease. Briefly, free fatty acid (FFA) flux could activate the transcriptional factors such as peroxisome proliferator-activated receptor gamma (PPARγ). In an aggravated state, this process promotes the increased production of reactive oxygen species (ROS) and aberrant levels of pro-inflammation markers such as tumor necrosis factor-alpha (TNF-α), the nuclear factor kappa B (NF-κB) and transforming growth factor beta (TGFβ-1). SREBP1c = sterol regulatory element-binding protein; TG = triglycerides; ROS = reactive oxygen species; IL-6 = interleukin 6; VLDL = very low-density lipoproteins.