DO treatment alleviated microbiota dysbiosis and reduced the abundance of the LPS-producing bacteria, Proteobacteria, Sutterella, and Escherichia-Shigella, reduced the abundance of the intestinal barrier-disrupting bacteria, Turicibacter, Ruminococcus, decreased intestinal permeability to reduce the movement of gut-derived LPS from the portal vein blood into the liver, inhibiting hepatic TLR4 activation and NF-κB nuclear translocation, and improving hepatic inflammation and steatosis to prevent NASH. The gene discussed is TLR4; the disease is steatosis.