| Objective: An intestine ischemic reperfusion (IR) rat model was adopted to investigate the effects of changes of gut mucosal immune function to bacterial and endotoxic translocation after intestine IR injury. Then the influence of α-melanocyte stimulating hormone (α-MSH) or dexamethasone on gut mucosal immune function and bacterial and endotoxic translocation after intestine IR injury was explored. The aim of this study was to gain more evidences of α-MSH contributing to preventing systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) after trauma or shock.Methods: One hundred and twenty Wistar rats were randomizedly divided into 5 groups, including sham IR group (SIR), IR group (IR), treated with 0.5mg/kg α-MSH after IR (SMSH), treated with 2.5mg/kg α-MSH after IR (LMSH) and treated with 2mg/kg dexamethason after IR (DEX). Rats in each group were killed at 0,2,6,24 hour after IR. Another 6 rats were chosen randomizedly as control group. The treated groups were injected 0.5mg/kg α-MSH, 2.5mg/kg α-MSH or dexamethason respectively into rat's caudal vein in 5 minutes before clamp and after IR. At different time point, the levels of secretory immunoglobulin A (sIgA), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in plasma and intestinal mucosal were measured by radioimmunoassay. Plasma endotoxin was determined by kinetic turbidimetric limulus test. The lymphocytic proliferation activity in gut-associated lymphoid tissue was assessed by MTT colorimetric assays. Simultaneously, bacterial translocation was examined and gut pathological changes were observed.Results: 1. Compared with SIR group, the level of sIgA in plasma and intestinal mucosal decreased significantly after IR. The level of TNF-α, IL-1β in plasma and intestinal mucosal increased at any time after IR, all of which reached the peak level 2hr or 6hr after IR(P<0.05).Simultaneously, the lymphocytic proliferation activity in gut-associated lymphoid tissue was depressed remarkably after IR(P<0.05). 2. It began to appear bacterial translocation in plasma and tissue extro-intestine 2hr after IR. Plasma endotoxin content in IR group was much higher than that of SIR group(P<0.05). Both of them negatively correlated to the decrease of the lymphocytic proliferation activity in gut-associated lymphoid tissue and the level of sIgA in plasma and intestinal mucosal(r=-0.534~-0.803,P<0.01). 3. Intestinal mucosa damage was noticed 6hr after IR. Mucosal degeneration and necrosis were the main expressions under microscope. α-MSH and dexamethason both improved ultrastructure of small intestine tissue evidently. 4. Compared with IR group, both 0.5mg/kg and 2.5mg/kg α-MSH significantly reduced the levels of TNF-αand IL-6, which averagely flown down about 17%~21%. The level of sIgA increased in SMSH and LMSH group, which elevated about 35%~47% in plasma at 6hr and 35%~38% in intestinal mucosal at 2hr(P<0.01). Furthermore, the lymphocytic proliferation activity also increased and endotoxin bacterial translocation was depressed in SMSH and LMSH group compared with IR group. There was no significant difference between SMSH and LMSH group(P>0.05).5. Compared with IR group, dexamethason remarkably suppressed the levels of TNF-αand IL-6, which averagely flown down about 38%~45%(P<0.01). Furthermore ,the level of sIgA was also averagely flown down about 15%~25%(P<0.05)and the lymphocytic proliferation activity was obviously inhibited in DEX group(P<0.05). Endotoxin bacterial translocation wasn't depressed in DEX group compared with IR group(P>0.05).Conclusions: 1. Gut mucosal immune function appears two phases' changes after IR. Inflammatory cytokines such as TNF-αand IL-6 are massy activated. On the other hand, gut mucosal immune function is obviously inhibited. There should be relationships between the disorder of gut mucosal immune function and endotoxin bacterial translocation. 2.α-MSH can improve gut mucosal immune function, relieve gut mucosa edema and inhibit endotoxin bacterial translocation.
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