In wild-type and loss-of-function TLR4-mutant mice fed with HFD, green tea extract (2% in diet, 8 weeks) protected against inflammation in NASH, which was likely achieved by blocking the translocation of gut-derived endotoxin and TLR4/MYD88/NFκB activation, followed with lowered phosphorylation of the NF-κB p65 subunit and gene expressions of pro-inflammatory factors (TNF-α, MCP-1, MPO, and iNOS/inducible nitric oxide synthase) [138]. Here, MPO is linked to metabolic dysfunction-associated steatohepatitis.