Dynamic changes of IL-2/IL-10, sFas and expression of Fas in intestinal mucosa in rats with acute necrotizing pancreatitis
Dynamic changes of IL-2/IL-10, sFas and expression of Fas in intestinal mucosa in rats with acute necrotizing pancreatitis
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DOI：
10.3748/wjg.14.2246
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发表时间：
2008-04-14
影响因子：
4.3
通讯作者：
Zhu, Bei
中科院分区：
文献类型：
--
作者：
Dang, Sheng-Chun;Zhang, Jian-Xin;Zhu, Bei
目的：探讨急性坏死性胰腺炎大鼠血清IL-2、IL-10、IL-2/IL-10、sFas的动态变化。探讨急性坏死性胰腺炎（ANP）大鼠肠黏膜Fas表达情况。方法：64只SD大鼠随机分为2组：正常对照组（C组）、ANP组（P组）。通过胰膜下注射50 g/L牛磺胆酸钠诱导ANP模型。正常对照组同样方法等体积注射9 g/L生理盐水溶液。各组大鼠经肠系膜上静脉取血，测定IL-2、IL-10、sFas水平并计算IL-2/IL-10值。通过ELISA测定IL-2、IL-10和sFas的水平。通过病理评分评价肠黏膜损伤的严重程度。免疫组化染色检测肠粘膜组织Fas表达情况。 结果：P组血清IL-2水平显着高于C组（2.79±0.51v5±3.53±0.62、2.93±0.89 vs 4.35±1.11、4.81±1.23v5±6.94±分别为 1.55 和 3.41 +/- 0.72 vs 4.80 +/- 1.10，P < 0.01），并在 6 小时达到峰值。 P组6 h和12 h血清IL-10水平显着高于C组（54.61+/-15.81v547.34+/-14.62、141.15+/-40.21v5156.12+/-43.10、89.18+/-32.52 vs 494.98+/-分别为 11.23 和 77.15 +/- 22.60 与 93.28 +/- 25.81，所有 P < 0.01）。 P组IL-2/IL-10值在0.5 h和2 h时显着高于C组（分别为0.05±0.01 vs 0.07±0.02和0.02±0.01 vs 0.03±0.01，均P < 0.01），并且在6 h时显着低于C组（0.05±0.01）。 0.02 vs 0.01 +/- 0.01，P < 0.01）并在 12 小时时返回到控制水平（0.04 +/- 0.01 vs 0.05 +/- 0.02，P > 0.05）。在sFas测定中，P组和C组之间没有显着差异（3.16 +/- 0.75 vs 3.31 +/- 0.80、4.05 +/- 1.08 vs 4.32 +/- 1.11、5.93 +/- 1.52 vs 5.41 +/- 1.47和4.62 +/- 1.23 vs 4.44 +/- 1.16，P > 0.05，对于所有）。 P组与C组比较，P组病理改变明显加重。免疫组化染色显示，正常肠组织中不表达Fas，但在胰腺炎诱导后，肠组织中Fas表达逐渐增加，12 h达高峰。结论：Fas参与了胰腺炎相关肠损伤的发病机制。 Fas的机制可能与Fas介导的T辅助细胞凋亡有关。 (C) 2008 WJG。版权所有。
AIM: To investigate dynamic changes of serum IL-2, IL-10, IL-2/IL-10 and sFas in rats with acute necrotizing pancreatitis. To explore the expression of Fas in intestinal mucosa of rats with acute necrotizing pancreatitis (ANP).METHODS: A total of 64 Sprague-Dawley (SD) rats were randomly divided into two groups: normal control group (C group), ANP group (P group). An ANP model was induced by injection of 50 g/L sodium taurocholate under the pancreatic membrane. Normal control group received isovolumetric injection of 9 g/L physiological saline solution using the same method. The blood samples of the rats in each group were obtained via superior mesenteric vein to measure levels of IL-2, IL-10, sFas and calculate the value of IL-2/IL-10. The levels of IL-2, IL-10 and sFas were determined by ELISA. The severity of intestinal mucosal injury was evaluated by pathologic score. The expression of Fas in intestinal mucosal tissue was determined by immunohistochemistry staining.RESULTS: Levels of serum IL-2 were significantly higher in P group than those of C group (2.79 +/- 0.51 v5 3.53 +/- 0.62, 2.93 +/- 0.89 vs 4.35 +/- 1.11, 4.81 +/- 1.23 v5 6.94 +/- 1.55 and 3.41 +/- 0.72 vs 4.80 +/- 1.10, respectively, P < 0.01, for all) and its reached peak at 6 h. Levels of serum IL-10 were significantly higher in P group than those of C group at 6 h and 12 h (54.61 +/- 15.81 v5 47.34 +/- 14.62, 141.15 +/- 40.21 v5 156.12 +/- 43.10, 89.18 +/- 32.52 vs 494.98 +/- 11.23 and 77.15 +/- 22.60 vs 93.28 +/- 25.81, respectively, P < 0.01, for all). The values of IL-2/IL-10 were higher significantly in P group than those of C group at 0.5 h and 2 h (0.05 +/- 0.01 vs 0.07 0.02 and 0.02 +/- 0.01 vs 0.03 +/- 0.01, respectively, P < 0.01, for all), and it were significantly lower than those of C group at 6 h (0.05 +/- 0.02 vs 0.01 +/- 0.01, P < 0.01) and returned to the control level at 12 h (0.04 +/- 0.01 vs 0.05 +/- 0.02, P > 0.05). In sFas assay, there was no significant difference between P group and C group (3.16 +/- 0.75 vs 3.31 +/- 0.80, 4.05 +/- 1.08 vs 4.32 +/- 1.11, 5.93 +/- 1.52 vs 5.41 +/- 1.47 and 4.62 +/- 1.23 vs 4.44 +/- 1.16, respectively, P > 0.05, for all). Comparison of P group and C group, the pathological changes were aggravated significantly in P group. Immunohistochemistry staining show the expression of Fas was absent in normal intestinal tissues, however, it gradually increased after induction of pancreatitis in intestinal tissue, then reached their peaks at 12 h.CONCLUSION: Fas were involved in the pathogenesis of pancreatitis associated intestinal injury. The mechanisms of Fas may be associated to Fas mediated T helper cell apoptosis. (C) 2008 WJG. All rights reserved.