Previous research demonstrated that the metabolites of BZA or MA catalyzed by SSAO could also significantly decrease LPS-induced iNOS and cyclo-oxygenase-2 (COX-2) expression, as well as NO production, which might be useful for normalization of glucose disposal during endotoxemia [20], while its role in hemorrhagic shock are largely unknown. This evidence concerns the gene PTGS2 and serum lipopolysaccharide activity.