The current findings depicted that CLM markedly inhibited oxidative damage and inflammation in the liver because of sepsis via upregulating levels of KLA, GSH, and SOD and suppressed those of PCT, IL-18, MDA IL-1β, and TNFα, Furthermore, it mitigated apoptosis via downregulation of Bax, NF-kB, and caspase 3 genes while elevating Bcl-2 gene expression. The gene discussed is NFKB1; the disease is Sepsis.