Although the understanding of underlying mechanisms by which Gu-4 protects mice from endotoxemia and sepsis requires systemic investigation, our in vitro data support the hypothesis that Gu-4 inhibits the leukocyte-endothelial cell adhesion by modulation of the affinity and avidity of leukocyte integrin CD11b and alleviates the inflammatory response and organ injury, thereby providing therapeutic effects to animals. The gene discussed is ITGAM; the disease is serum lipopolysaccharide activity.