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The superior mesenteric artery occlusion (SMAO) shock caused byintestinal ischemia reperfusion (I/R) is a common critical clinicalpathological process in clinic, which often occurrs on shock resuscitation,post of organ transplantation or the treatment process of severe trauma, etc.SMAO shock may contribute to intestinal barrier dysfunction, bacteria/endotoxin translocation (BET), and lots of inflammatory mediator released,induced multiple organ dysfunction syndrome (MODS), even endangeredthe lives of patients. Therefore, it is worthwhile to explore the mechanismof systemtic remote organs injury and find effectively preventmentmeasures.As the development of research in intestinal lymphatic pathway, moreand more results show that it is critical for intestinal lymphatic pathway tothe pathogenesis of remote organs injury. Our former researchdemonstrated that mesenteric lymph reperfusion (MLR) may aggravatehistologic damage of lung, kidney, myocardium, liver on SMAO shock rats,the mechanism of which may relate to increased free radical damage andinflammation injury. To further investigate the mechanism of mesentericlymph reperfusion aggravating inflammatory response on SMAO shockrats, in this study, we take polymorphonuclear neutrophils (PMN), highmobility group protein box-1 (HMGB1), receptor of advanced glycationend-products (RAGE), nuclear factor-kappa B (NF-κB) as a starting point,to explore the mechanism of inflammaroty response that multiple factors’role of mesenteric lymph reperfusion aggravate organ injury SMAO rats,and provide experimental basis for prevention and treatment of SMAO shock.Tweenty-four Wistar male rats were randomly divided into fourgroups: in SMAO group, performed 1 hour (h) occlusion of superiormesenteric artery (SMA) and then followed by 2 h of reperfusion; in MLRgroup, performed 1 h occlusion of mesenteric lymphatic duct (MLD), andthen followed by 2 h of reperfusion; in SMAO+MLR group, performed 1hocclusion of SMA and MLD, and then followed by 2h of reperfusion; insham group, only anesthetized and operation. After 2h of reperfusion,myocardium, liver, lung and kidney were taken, a part were fastened byneutral formalin, embedded by paraffin, the section were determined theexpression of HMGB1, RAGE, NF-κB and myeloperoxidase (MPO) byimmunohistochemical (IHC) staining; the other of part were homogenizedas 16.7 percent, determined the contents of RAGE, intercellular adhesionmolecule-1 (ICAM-1) in enzyme-linked immunosorbent assay (ELISA).The results showed that each index in MLR group and sham group hasno statistical significance. The content of ICAM-1 and expressing of MPOof lung, kidney, liver and myocardium in SMAO group were higher thanthat in MLR group and sham group(P<0.05, P<0.01), and the content ofICAM-1 and expression of MPO in SMAO+MLR group were more or lesshigher than that in SMAO group, MLR group and sham group (P<0.05,P<0.01). These results reveals that the mechanism of MLR aggravatesinflammatory response in SMAO shock rats is related to the increase ofPMN in tissue. The content of RAGE and the expression of HMGB1 andRAGE of the lung, kidney, myocardium, liver in the SMAO group(P<0.05,P<0.01), SMAO+MLR were higher or stronger than the MLR and the shamgroup (P<0.05, P<0.01), and these indicators in SMAO+MLR group werehigher or stronger than that in SMAO group (P<0.05, P<0.01). The resultssuggested that the mechanism of MLR aggravates organs inflammatoryresponse of SMAO rats are related to the higher expression ofHMGB1(P<0.05, P<0.01). We also found that the NF-κBp65 expression of the SMAO group and SMAO+MLR group were significantly higher thanthe MLR group and sham group in the lung, kidney, myocardium, liver.And the NF-κBp65 expression of the SMAO+MLR group was strongerthan SMAO group in each tissues (P<0.05, P<0.01).The results showedthat increased expression of NF-κB involve in the mechanisms of MLRaggravate inflammatory response of rat organs in the SMAO shock.In summary, on the one hand, the expression of ICAM-1 increased inSMAO shock rats by MLR, which induced to PMN adhesion, PMN wereseized by tissue, excessively active PMN sharpen inflammatory response;on the other hand, MLR aggravated the expression of HMGB1, RAGE andNF-κB in SMAO shock rats. At the same time, the level of RAGE wereincreased. So, inflammatory response aggravated by HMGB1, RAGE orNF-κB. As for the relations among HMGB1, RAGE, NF-κB and theinteraction of three factors in MLR aggeravated inflammatory response toSMAO shock rats must be further verification in future.
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