论文部分内容阅读
目的:探讨NO及TNF-α在实验性慢性末端回肠炎发病过程中的作用。方法:清洁级SD大鼠,随机分为造模组、缝线组、对照组。测血清NO的浓度,取大鼠回肠末端组织,进行HE染色观察病理组织学变化,RT-PCR检测TNF-α的表达。结果:病理:2周时造模组与缝线组末端回肠均出现急性炎症表现。造模组8周为慢性炎症反应期。缝线组8周与对照组无差异性。造模组血清中NO浓度高于对照组及缝线组,且随着病程的延长明显增加;NO浓度与镜下炎症评分呈正相关,术后2W及8W时,造模组较对照组表达水平高,2周时,造模组与缝线组NO浓度无显著性差异,8周时,造模组与缝线组明显高于缝线组。造模组末端回肠组织TNF-α的表达水平在术后8W与2W时相比差异有统计学意义,与缝线组及对照组相比均有显著性差异。结论:CTI发病过程中,血清NO浓度增加,且与炎症程度呈正相关,TNF-α表达随着时间延长明显增加。表明NO及TNF-α在CTI的发病中可能起着一定的作用。
Objective: To investigate the role of NO and TNF-α in the pathogenesis of experimental chronic terminal ileitis. Methods: Clean SD rats were randomly divided into model group, suture group and control group. The concentration of serum NO was measured. The terminal ileum tissue of rats was taken for HE staining to observe the histopathological changes. The expression of TNF-α was detected by RT-PCR. Results: Pathology: Acute inflammation appeared in the terminal ileum of model group and suture group at 2 weeks. The model group was chronic inflammatory reaction for 8 weeks. Suture group 8 weeks and no difference between the control group. The concentration of NO in the model group was higher than that in the control group and the suture group, and with the prolongation of the course, the NO concentration was positively correlated with the inflammation score. The expression of NO in the model group was significantly higher than that in the control group at 2W and 8W At 2 weeks, there was no significant difference in NO concentration between the model group and the suture group. At 8 weeks, the model group and the suture group were significantly higher than the suture group. The expression level of TNF-α in the terminal ileum of the model group was significantly different at 8W and 2W postoperatively, which was significantly different from that of the suture group and the control group. CONCLUSIONS: During the onset of CTI, the concentration of serum NO increased, and it was positively correlated with the degree of inflammation. The expression of TNF-α increased significantly with time. That NO and TNF-α in the pathogenesis of CTI may play a role.