NFKB1 and serum lipopolysaccharide activity: As previously demonstrated in mice with LPS-induced cardiac failure, inflammatory signaling mediated by transcription factors (NF-κB and AP-1) and stress-activated mitogen activated protein (MAP) kinases were augmented to enhance cytokine production in endotoxemia [22] and AR inhibitor effectively reduced such signaling and thereby suppressed cytokine production.