NFKB1 and sexually transmitted disease: XQAS treatment dose-dependently inhibited hypoexpression of IκBα in the cytosol, hyperexpression of NF-κB p65 mRNA, and hypoexpression in the cytosol with hyperexpression in the nuclei of NF-κB p65 in the injured muscle, suggesting that XQAS can inhibit acute STI-induced IκBα degradation, overexpression of NF-κB p65 gene, and NF-κB p65 translocation into nuclei from cytosol, all of which results in an inhibition in activated inflammatory signaling pathway.