In the animal studies, CYY054c alleviated LPS-upregulated plasma TNF-α, IL-1β, IL-6, and NO concentrations, as well as cardiac monocyte chemotactic protein-1, iNOS, and COX-2 expression in rats, contributing to the improvement of cardiac function during endotoxemia.
Our data suggest that an activation of the COX-2/mPGES-1 synthetic pathway is responsible for the increased renal formation of PGE<sub>2</sub> in response to LPS and that the vasodilatory effect of PGE<sub>2</sub> and PGI<sub>2</sub> is enhanced during endotoxemia.
In an LPS-induced endotoxemia mouse model, pretreatment with EPS reduced the mRNA levels of inducible nitric oxide synthase, cyclooxygenase-2 and proinflammatory cytokines and increased the survival rate of mice.