Yao et al found that dioscin reduced the overexpression of TLR4 and myeloid differentiation primary response gene 88 in LPS-induced inflammatory mice and rats, resulting in a significant reduction in the levels of downstream inflammatory factors, such as TRAF6, p-NFκB, IL-1β, IL-6, and TNF-α, which in turn reduced inflammatory injury.[16] Tsukayama et al demonstrated that diosgenin inhibits COX2 expression in human non-small cell lung cancer A549 cells and downregulates COX2 and prostate E2 synthase-1 (mPGES-1) expression in a mouse model of lipopolysaccharide (LPS)-induced liver injury. This evidence concerns the gene NFKB1 and non-small cell lung carcinoma.