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目的:研究肠系膜淋巴再灌注对肠系膜上动脉闭塞性(SMAO)休克大鼠肺部炎症反应的影响。方法:24只Wistar雄性大鼠均分为4组:SMAO组,MLR组,SMAO+MLR组,SHAM组。再灌注2h后,迅速留取肺组织,一部分制备组织匀浆,检测细胞间粘附分子(ICAM-1)和晚期糖基化产物受体(RAGE)。再另外选取固定位置肺部组织放入中性甲醛中固定,用于测定肺内HMGB1、RAGE的表达。结果:SMAO与SMAO+MLR组肺部组织匀浆ICAM-1、RAGE含量显著高于MLR与SHAM组,且SMAO+MLR组肺组织匀浆的ICAM-1、RAGE含量高于SMAO组。肺部组织内HMGB1和RAGE在MLR组与SHAM组基本不表达,或少量表达,MLR加重了SMAO休克模型中HMGB1和RAGE的表达。结论:MLR加重SMAO休克大鼠肺部炎症反应,进一步证实肠淋巴途径在SMAO休克发病学中具有重要作用,同时证实HMGB1及RAGE在SMAO休克大鼠的炎症失常反应中起重要作用。
Objective: To investigate the effect of mesenteric lymph reperfusion on inflammatory reaction in the lung of rats with superior mesenteric artery occlusion (SMAO). Methods: Twenty-four Wistar male rats were divided into 4 groups: SMAO group, MLR group, SMAO + MLR group and SHAM group. After reperfusion for 2h, lung tissue was collected rapidly and part of tissue homogenate was prepared for detection of intercellular adhesion molecule (ICAM-1) and advanced glycation receptor (RAGE). In addition to select a fixed location of the lung tissue fixed in neutral formaldehyde for determination of lung HMGB1, RAGE expression. Results: The levels of ICAM-1 and RAGE in the lung homogenates in SMAO and SMAO + MLR groups were significantly higher than those in MLR and SHAM groups, while the contents of ICAM-1 and RAGE in lung homogenates of SMAO + MLR group were higher than those in SMAO group. The expression of HMGB1 and RAGE in the SMAO shock model was significantly increased in the lung tissue with little or no expression of HMGB1 and RAGE in MLR group and SHAM group. Conclusions: MLR aggravates pulmonary inflammatory response in rats with SMAO shock, and further confirms that intestinal lymph pathway plays an important role in the pathogenesis of SMAO shock. HMGB1 and RAGE also play an important role in inflammatory disorders in SMAO shock rats.