目的观察丙氨酰—谷氨酰胺双肽对缺血/再灌注损伤兔肠道黏膜损伤后中性粒细胞浸润及黏膜组织中炎性反应水平的影响。方法选择健康成年新西兰兔30只,按随机数字表法分为治疗组与对照组各15只。采用完全夹闭阻断肠系膜上动脉1h后再开放恢复肠系膜上动脉血流方法制作缺血/再灌注肠损伤模型后,治疗组健康成年新西兰兔肠缺血/再灌注肠损伤模型建立前2h及模型建立后2h,通过耳缘静脉分别给予丙氨酰—谷氨酰胺双肽1次,剂量为1.0g/kg。对照组同期相同时间点分别给予等量的葡萄糖生理盐水静脉注射。缺血/再灌注模型成功后4小时,空气栓塞法处死新西兰兔。苏木素—伊红染色光镜下观察损伤肠组织的病理学变化,依据Chiu 6级评分法计算肠损伤程度评分。测量小肠黏膜组织中肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)水平变化。取肠系膜上静脉血进行中性粒细胞计数(PMN),测定PMN呼吸爆发的强度变化。结果缺血/再灌注损伤兔模型建立后,对照组肠道黏膜肉眼观小肠黏膜充血、肿胀,可见斑点状糜烂,部分见炎性渗出物,光镜下肠壁组织间中性粒细胞浸润,血管内皮肿胀,基底层结构不清。小肠绒毛数量减少,高度降低,形态不规则,肠上皮黏膜细胞大小不一,排列紊乱,黏膜层厚度变薄,隐窝结构不清楚,小肠腺体萎缩。观察组小肠黏膜充血、肿胀明显减轻,未见点状或片状糜乱。光镜下小肠绒毛数量未见明显减少,形态基本正常,黏膜层厚度正常及基底层结构清晰,炎性细胞浸润较少。治疗组的肠损伤程度评分为(2.15±0.93)分低于对照组的(4.98±0.85)分,治疗组TNF-α、IL-6水平明显低于对照组,PMN低于对照组,差异均有统计学意义(P<0.05)。结论丙氨酰—谷氨酰胺双肽能减少缺血再灌注损伤后肠黏膜中性粒细胞浸润程度,减轻中性粒细胞活化强度,保护肠黏膜屏障功能。其机制可能与降低了损伤肠壁中TNF-α与IL-6水平,抑制了肠壁氧化应激反应引起的炎性反应损伤,降低了肠壁毛细血管通透性有关。 Objective To observe the effect of alanyl-glutamine dipeptide on neutrophil infiltration and inflammatory reaction in mucosal tissue after intestinal mucosal injury in rabbits with ischemia / reperfusion injury. Methods Thirty healthy adult New Zealand rabbits were randomly divided into treatment group (n = 15) and control group (n = 15) according to random number table. After occlusion of the superior mesenteric artery for 1h and then the recovery of superior mesenteric artery blood flow were used to make the model of intestinal injury after ischemia / reperfusion, the intestinal injury model of intestinal ischemia / reperfusion in healthy adult New Zealand white rabbits was established 2h before and Two hours after the establishment of the model, alanyl-glutamine peptidase was given through the ear vein at a dose of 1.0 g / kg. Control group at the same time point were given the same amount of glucose saline intravenously. Four hours after the successful ischemia / reperfusion model, New Zealand rabbits were sacrificed by air embolism. The pathological changes of intestinal tissue were observed under hematoxylin-eosin staining, and the score of intestinal injury was calculated according to Chiu 6-grade score. The changes of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in intestinal mucosa were measured. Mesenteric venous blood was taken for neutrophil count (PMN), and the intensity of PMN respiratory burst was measured. Results After establishment of the rabbit model of ischemia / reperfusion injury, the intestinal mucosa in the control group was hyperemic and swollen with speckled erosions. Some inflammatory exudates were observed. The neutrophil infiltration , Vascular endothelial swelling, unclear basal layer structure. Intestinal villi reduce the number of highly reduced, irregular shape, intestinal epithelial mucosal cells of different sizes arranged disorder thinning mucosal layer thickness, crypt structure is not clear, small intestine gland atrophy. Observation group of small intestinal mucosa congestion, swelling was significantly reduced, no punctate or patchy. Under the light microscope, there was no obvious decrease in the number of small intestine villi, the morphology was basically normal, the thickness of mucosal layer was normal, the structure of basal layer was clear, infiltration of inflammatory cells was less. The score of intestinal injury in the treatment group was (2.15 ± 0.93) points lower than that in the control group (4.98 ± 0.85) points, and the levels of TNF-α and IL-6 in the treatment group were significantly lower than those in the control group There was statistical significance (P <0.05). Conclusion Alanyl-glutamine dipeptide can reduce the intestinal mucosal neutrophil infiltration, reduce the activation intensity of neutrophils and protect the intestinal mucosal barrier function after ischemia-reperfusion injury. The mechanism may be related to reducing the level of TNF-α and IL-6 in the injured intestinal wall, inhibiting the inflammatory reaction damage caused by oxidative stress in the intestinal wall and reducing the capillary permeability of the intestinal wall.