Green tea extract (GTE) protects against nuclear factor kappa B (NFkappaB)-mediated liver inflammation during nonalcoholic steatohepatitis (NASH). However, the mechanisms by which GTE exerts its antiinflammatory activities during NASH are unclear. There are several potential pathways and environmental conditions that mediate hepatic NFkappaB activation during NASH, including intracellular oxidative stress that is downregulated by nuclear factor E2-related factor 2 (Nrf2)-dependent antioxidant defenses, as well as the extracellular receptor-mediated pathways toll-like receptor 4 (TLR4) and tumor necrosis factor receptor 1 (TNFR1). Therefore, this dissertation aimed to define the involvement of these pathways in relation to antiinflammatory activities of GTE on hepatic NFkappaB activation during NASH. The central hypothesis was that GTE suppresses hepatic NFkappaB activation by increasing the activities of Nrf2, and by decreasing TLR4- and TNFR1-mediated signaling. Contrary to the hypothesis, studies in Nrf2-knockout mice demonstrated that GTE exerts its antiinflammatory activities against NFkappaB activation during NASH in an Nrf2-independent manner. Studies in wild-type mice that were fed with low-fat (LF) or high-fat (HF) diet containing 0 or 2% GTE demonstrated that GTE lowers NFkappaB-dependent inflammatory responses by reducing ligand availability for, and receptor expression of, TNFR1 and TLR4 pathways. Also, GTE protects against metabolic endotoxemia by restoring intestinal tight junction protein expression. Lastly, studies in loss-of-function TLR4-mutant mice showed that GTE exerts it antiinflammatory activities at the liver in a TLR4-dependent manner, whereas intestinal-level benefits are mediated in a TLR4-independent manner. These findings are of significance in that they provide evidence to support GTE as a dietary strategy for NASH, specifically inflammation that mediates hepatic injury. These findings also provide basis for future clinical trials on the preventive and therapeutic potentials of GTE in mitigating liver inflammation during NASH.