急性胰腺炎大鼠的炎性因子及胃黏膜的变化观察

目的观察急性胰腺炎的炎性因子表达,并且重点分析炎性因子与胃黏膜病变之间的发生机制。方法选取SD大鼠64只,随机分为模型组和对照组(假手术组)。造模后2 h和12 h后分别各取8只动物经肠系膜上静脉采血,检测血清TNF-α、IL-1和核转录因子κB(NF-κB)表达水平;测定胃黏膜血流和损害情况及NF-κB蛋白活化水平。采用SPSS 17.0和Excel 2007软件进行统计分析,实验数据用均数±标准差(x珋±s)表示,炎性细胞因子和胃粘膜血流量(GMBF)等数据的组间比较采用成组t检验,P0.05为差异有统计学意义。结果模型组建模后2 h的TNF-α、IL-1水平显著高于建模前和对照组(P0.05)。模型组建模后12 h的NF-κB、TNF-α、IL-1水平显著高于建模前和对照组(P0.05)。模型组造模后2 h出现出轻微的泡壁水肿,但无炎细胞浸润,无出血发生。12 h后观察到黏膜充血、水肿、粗糙不平,点状出血、淤点或淤斑,点状或者斑片状糜烂,黏膜可见血管显露或者是粗大皱襞及结节。模型组的GMBF表达量与血清NF-κB表达水平之间呈密切负相关(P0.05)。而与TNF-α、IL-1无相关性(P0.05)。结论炎症介导了NF-κB的活化,导致了胃黏膜局部缺血发生,并最后导致了胃黏膜的损伤。而且NF-κB的活化同时也在不断的反向调节TNF-α、IL-1的升高,加重了急性胰腺炎的发展。

Experimental observation of serum inflammatory cytokines and gastric mucosa changes of rats with acute pancreatitis

Objective To observe the expression of inflammatory cytokines in acute pancreatitis , and to analyze the mechanism of inflammatory factors and gastric mucosal lesions . Methods 64 SD rats were randomly divided into model group and control group (sham operation group).After 2 h and 12 h, 8 animals were taken from the superior mesenteric vein, and the expression levels of TNF-α, IL-1 and NF-κB were detected. Determination of blood flow and damage of gastric mucosa and the level of NF-κB protein activation.SPSS 17.0 and Excel 2007 software were used for statistic analysis, experiment data were represent as (x-±s).The inflammatory cytokines and gastric mucosal blood flow were examined by group t test, P<0.05 was statistically different. Results At 2 h after modeling, The TNF-αand IL-1 levels of model group were significantly higher than those of the control group (P<0.05).At 12 h after modeling, The NF-κB, TNF-αand IL-1 levels of model group were significantly higher than those of the control group (P<0.05).In the model group, there was a slight edema of the bubble wall, but no inflammatory cell infiltration, no bleeding occurred at 2 h after modeling.At 12 h after modeling, mucosal hyperemia, edema, rough, dotted hemorrhage, silting point or ecchymosis, dotted or patchy erosion, mucous membrane visible blood vessels or bulky fold and nodules were observed .There was a close negative correlation between the expression of GMBF in the observation group and the expression level of NF-κB in the serum ( P <0.05 ).And with TNF-α, IL-1 no correlation ( P >0.05 ). Conclusion Inflammation mediates the activation of NF-κB, which leads to the occurrence of gastric mucosal ischemia and the injury of gastric mucosa.In the same time, the activation of NF-κB and the increase of IL-1 and TNF-αin the reverse regulation, aggravated the development of acute pancreatitis.