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下丘脑白介素-6对应激性溃疡大鼠胃黏膜损伤的影响
引用本文:钱俊,卢亦成,于明琨. 下丘脑白介素-6对应激性溃疡大鼠胃黏膜损伤的影响[J]. 中华急诊医学杂志, 2010, 19(9). DOI: 10.3760/cma.j.issn.1671-0282.2010.09.010
作者姓名:钱俊  卢亦成  于明琨
作者单位:第二军医大学附属长征医院神经外科,上海,200003
基金项目:军队"十一五"资助项目 
摘    要:目的 探讨下丘脑白介素-6对应激性溃疡大鼠胃黏膜血流量、胃液pH值和胃黏膜损伤的影响.方法 采用液压打击法建立大鼠颅脑外伤应激性溃疡模型.20只雄性SD大鼠在长征医院神经外科大鼠实验房饲养1周后开始实验.大鼠被随机(随机数字法)等分为对照组、致伤1 h组、致伤6h和致伤12 h组,采用免疫组化、Western blot等方法检测致伤后下丘脑性白介素-6的表达与分布.同时,检测各组大鼠胃液pH值、胃黏膜血流量、胃黏膜损伤指数,并观察胃黏膜大体及光镜下组织病理学变化.结果 白介素-6免疫反应阳性细胞广泛分布于应激大鼠下丘脑水平的神经细胞中,在室旁核(paraventricular rucleus,PVN)附近分布尤为密集.致伤后1h胃液pH值明显降低,致伤后6 h处于最低点(与1 h组比较P<0.05).致伤后1 h即出现胃黏膜损伤,并且胃黏膜损伤指数随时间的延长而不断增加;致伤后1 h有血流量的暂时性增加,处于波峰,6 h后趋于平稳.大体及镜下病理均提示,胃黏膜呈应激性溃疡改变.结论 在液压打击致应激性溃疡的SD大鼠中,下丘脑白介素-6可通过PVN的介导激活神经内分泌代谢,引发胃黏膜损伤.

关 键 词:脑损伤  液压模型  大鼠  免疫组化  白介素-6  应激性溃疡

Effects of interleukin-6 in hypothalamus on gastric mucosal injury in rats with stress ulcer
QIAN Jun,LU Yi-cheng,YU Ming-kun. Effects of interleukin-6 in hypothalamus on gastric mucosal injury in rats with stress ulcer[J]. Chinese Journal of Emergency Medicine, 2010, 19(9). DOI: 10.3760/cma.j.issn.1671-0282.2010.09.010
Authors:QIAN Jun  LU Yi-cheng  YU Ming-kun
Abstract:Objective To clarify the role of hypothalamic IL-6 in gastric mucosal blood flow, gastric juice pH value and gastric mucosal injury. Method Model of gastric stress ulcer was established by fluid percussion to make craniocerebral trauma. Twenty male SD rats fed for one week in the experiment room were randomly(random number) divided into control group, one hour group, six hours group and 12 hours group after injury. The levels and distribution of IL-6 in hypothalamus were detected by using immunohistochemistry and Western blot. Simultaneously, gastric pH value, gastric mucosal blood flow and gastric mucosal injury index of rats in each group were measured, and the histology of gastric mucosa was observed. Results IL-6 immunoreactive cells were widely distributed in neuronal cells of hypothalamus of the stressed rats especially in the para-ventricular nucleus (PVN).One hour after injury, the pH value rapidly declined, and the lowest point appeared 6 hours later. One hour after injury, the injury of gastric mucosa was found, and the injury became worse and worse as time got longer and longer. The ulcer index (UI) was increased. One hour after injury, there was a brief increase in blood flow to the peak in gastric mucosa, and then the blood flow declined until 6 hours elapsed and got stable. The experiment prompted the gastric stress ulcer appeared. Conclusions In the SD rats with gastric stress ulcer induced by craniocerebral injury incurred by hydraulic percussion, the hypothalamic IL-6 may activate neuronendocrine metabolism mediated through the activation of PVN, inducing gastric mucosal injury.
Keywords:Brain injury  Fluid-percussion model  Rat  Immunohistochemistry  IL-6  Stress ulcer
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