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目的通过建立实验性重症急性胰腺炎大鼠模型,谷氨酰胺灌胃,以期寻求谷氨酰胺在重症急性胰腺炎时的肠道保护作用及其分子机制。方法雄性SD大鼠90只,随机分为三组:假手术组、SAP组、谷氨酰胺治疗组。检测血浆D-乳酸OD值;免疫组化技术分析小肠组织ICAM-1的表达和肠黏膜细胞凋亡(TUNEL法)情况。结果SAP组在术后24 h、48 h和72 h各点血浆D-乳酸OD值均明显高于OP组,同时也高于谷氨酰胺治疗组。造模后24 h、48 h和72 h,SAP组肠组织血管内皮细胞ICAM-1表达光密度值与OP组相比明显增高。与谷氨酰胺治疗组相比,SAP组的ICAM-1的表达则有所下降。肠黏膜组织在SAP组发生细胞凋亡的数目与OP组相比明显增加。而谷氨酰胺治疗组与SAP组比较,细胞凋亡数目则有所降低。结论重症急性胰腺炎时肠黏膜屏障功能的损伤受多种因素的调节,而谷氨酰胺作为肠道的能源物质,对重症急性胰腺炎时肠黏膜屏障功能的破坏具有明显的保护作用。
Objective To establish a rat model of experimental severe acute pancreatitis, glutamine gavage, in order to seek the gutamide in severe acute pancreatitis intestinal protective effect and its molecular mechanism. Methods 90 male SD rats were randomly divided into three groups: sham operation group, SAP group and glutamine treatment group. The plasma D-lactate OD value was measured. The expression of ICAM-1 in small intestine tissue and the apoptosis of intestinal mucosa (TUNEL) were analyzed by immunohistochemistry. Results In the SAP group, the plasma D-lactate OD value at 24 h, 48 h and 72 h after operation were significantly higher than those in the OP group and also higher than those in the glutamine group. Compared with OP group, the optical density of ICAM-1 expression in the vascular endothelial cells of SAP group was significantly increased at 24 h, 48 h and 72 h after modeling. Compared with the glutamine treatment group, the expression of ICAM-1 in SAP group decreased. The number of apoptosis in intestinal mucosa in SAP group was significantly higher than that in OP group. However, the number of apoptotic cells in the glutamine treatment group was lower than that in the SAP group. Conclusion The damage of intestinal mucosal barrier function in severe acute pancreatitis is regulated by many factors. However, glutamine, as the energy substance of intestinal tract, has a significant protective effect on the damage of intestinal mucosal barrier function in severe acute pancreatitis.