The Pathogenic Effects Of PMNs Adhesion On SIRS And MODS And The Treatment By Emodin

Background: Systemic inflammatory response syndrome(SIRS) is aclinical acute disease and (or) severe disease that is inflammatory of totalbody caused by kinds of infectious or noninfectious major injury. In theprocess of SIRS pathophysiology, much ingredient of damage can induceexcessive stress response of body and activate immune cells, which enlargethe inflammatory reaction in cascade mod and can formatted vicious cycle,finally will lead to SIRS and multiple organ dysfunction syndrome(MODS).As a kind of immune cells ,PMNs overactivation plays animportant role in the occurrence and development of SIRS.MODS is thedeteriorating phase of SIRS ,which has become the major cause of death .Inorder to decrease the mortality of patients suffering from acute disease andsevere disease and guard against the occurrence of MODS ,the preventionof occurrence and development of SIRS is thought to be a key. More andmore attentions will be paid to the key stone of studying SIRSpathophysiological process and seeking effective therapeutic measures. Objectives: This research would investigate (1)the status of PMNsadhesion to endothelial cells ;(2)the influence of the serum of SIRS patientson endothelial cells;(3)the influence and mechanism of emodin on PMNsadhesion to endothelial cells and the activation of endothelial cells. Methods:21 patients with SIRS were enlisted in this study .All thepatients were divided into two group ,one group was diagnosed as simplySIRS, the other group was diagnosed as SIRS accompanying MODS.10healthy individuals were selected as normal control. All patients hadAPACHE Ⅱ scores assessed .Peripheral blood was obtained within24h.Serum concentration of TNF-αwas examined by radioimmunoassaymethod Plasma endotoxin was measured using a quantitative chromogenicLAL test. PMNs was isolated from peripheral blood.ECV-304 were treatedwith all groups serum. using emodin to treat the SIRS and MODS group for4h,then NF-κB,E-selectin was evaluated by western-blot in one part, at thesame time, the other part administrated by all groups of PMNs for15min,the ratio of adhesion was measured. Results: SIRS group compared with normal group, MODS groupcompared with SIRS group , plasma endotoxin ,serum TNF-αand PMNsadhesion ratio were significantly increased. SIRS and MODS group treatedwith emodin compared with SIRS and MODS group,the PMNs adhesion ratiowere significantly decreased. The expression of NF-κB, E-selectin weresignificantly increased in the endothelia cells treated by the serum of SIRS orMODS group, while in the emodin groups were significantly decreased. Conclusion: 1.Endotoxin, TNF-α might play important roles in the pathogenesis ofSIRS. 2.The activation of PMNs (The PMNs adhesion ratio is increased)and endothelial cells(The expression of E-selectin and NF-κB is enhanced)were the major pathophysiological changes of SIRS. 3.The PMNs adhesion ratio was inhibited by emodin ,which may beassociated with the deceased expression of E-selectin and NF-κB.