Experimental acute pancreatitis results in increased blood-brain barrier permeability in the rat:: a potential role for tumor necrosis factor and interleukin 6
Experimental acute pancreatitis results in increased blood-brain barrier permeability in the rat:: a potential role for tumor necrosis factor and interleukin 6
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DOI：
10.1016/s0304-3940(98)00060-3
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发表时间：
1998-02-20
影响因子：
2.5
通讯作者：
Abrahám, CS
中科院分区：
文献类型：
--
作者：
Farkas, G;Márton, J;Abrahám, CS
胰性脑病是急性胰腺炎的严重并发症。促炎细胞因子可能在胰腺炎多器官衰竭的发生发展中起一定作用。本研究测定了大鼠急性胰腺炎前、后6、24、48h血脑屏障(BBB)通透性的变化，同时测定了血清肿瘤坏死因子(TNF)和白介素6(IL-6)的水平。用特定的细胞系(WEHI-164用于肿瘤坏死因子，B-9用于IL-6)生物测定细胞因子浓度，用分光光度法测定顶叶皮质、海马、纹状体、小脑和延髓的血脑屏障通透性，小的(荧光素钠，相对分子质量376Da)和大的(伊文氏蓝白蛋白，相对分子质量67000 Da)。急性胰腺炎后6、24 h血清肿瘤坏死因子水平显著升高(P<；0.05)，24、48 h血清IL-6水平显著升高(P<；0.05)，两种示踪剂在急性胰腺炎动物不同脑区血脑屏障通透性均显著升高(P<；0.05)。我们认为，细胞因子，如肿瘤坏死因子和白介素6，可能参与了急性胰腺炎时血管源性脑水肿的形成。(C)1998年爱思唯尔爱尔兰科学有限公司。
Pancreatic encephalopathy is a severe complication of acute pancreatitis. Proinflammatory cytokines may play a role in the development of multi-organ failure during pancreatitis. In the present study, we measured the changes in the blood-brain barrier (BBB) permeability concomitantly with the determination of serum tumor necrosis factor (TNF) and interleukin-6 (IL-6) levels in rats before, as well as 6, 24 and 48 h after the beginning of intraductal taurocholic acid-induced acute pancreatitis. Cytokine concentrations were measured in bioassays with specific cell lines (WEHI-164 for TNF and B-9 for IL-6), while the BBB permeability was determined for a small (sodium fluorescein, molecular weight (MW) 376 Da), and a large (Evans' blue-albumin, MW 67 000 Da) tracer by spectrophotometry in the parietal cortex, hippocampus, striatum, cerebellum and medulla of rats. The serum TNF level was significantly (P < 0.05) increased 6 and 24 h after the induction of pancreatitis, while the IL-6 level increased after 24 and 48 h. A significant (P < 0.05) increase in BBB permeability for both tracers developed at 6 and 24 h in different brain regions of animals with acute pancreatitis. We conclude that cytokines, such as TNF and IL-6, may contribute to the vasogenic brain edema formation during acute pancreatitis. (C) 1998 Elsevier Science Ireland Ltd.