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目的:通过测定不同组大鼠脑缺血/再灌注损伤模型中脂多糖应答分子(LRG)表达水平的变化与炎症因子含量及大鼠脑梗死容积之间的关系,探讨内毒素重复预处理诱导脑保护效应的机制。方法:将66只SD大鼠随机分为假手术组、缺血对照组和内毒素预处理组,每组22只。采用戊巴比妥钠(40 mg/kg)腹腔注射麻醉大鼠,采用大鼠大脑中动脉栓塞模型(MCAO)制备大鼠大脑缺血/再灌注模型。采用免疫印迹法结合图像分析软件半定量计算LRG分子表达水平的变化,酶联免疫法测定脑组织TNF-α、IL-1β、IL-6、IL-10的含量,用氯化三苯四唑(TTC)染色法和计算机图像分析系统计算大鼠大脑梗死容积。结果:相比于缺血对照组,内毒素重复预处理组大鼠大脑LRG分子表达水平明显上调,TNF-α、IL-1β、IL-6含量明显降低,IL-10的含量明显增高,同时,内毒素预处理组较缺血对照组神经功能评分明显升高,脑梗死容积明显缩小。结论:内毒素重复预处理通过上调LRG分子表达,促进致炎-抑炎因子之间的动态平衡介导脑保护作用。
OBJECTIVE: To investigate the relationship between the changes of LRG expression and the content of inflammatory cytokines and the volume of cerebral infarction in different groups of rats with cerebral ischemia-reperfusion injury Mechanism of brain protection effect. Methods: Sixty-six SD rats were randomly divided into sham operation group, ischemia control group and endotoxin pretreatment group, with 22 rats in each group. The rats were anesthetized by sodium pentobarbital (40 mg / kg) intraperitoneally and the rat model of cerebral ischemia / reperfusion was established by middle cerebral artery occlusion model (MCAO). Western blotting and image analysis software were used to semi-quantitatively calculate the expression of LRG. The levels of TNF-α, IL-1β, IL-6 and IL-10 in brain tissues were determined by enzyme-linked immunosorbent assay (TTC) staining and computerized image analysis system to calculate cerebral infarct volume in rats. Results: Compared with the ischemic control group, the expression of LRG in the rat brain of endotoxin-treated group was significantly increased, the levels of TNF-α, IL-1β and IL-6 were significantly decreased and the content of IL-10 was significantly increased Compared with the ischemic control group, the neurological function score of endotoxin preconditioning group was significantly increased, and the cerebral infarction volume was significantly reduced. Conclusions: Endotoxin preconditioning can mediate cerebral protection by up-regulating the expression of LRG and promoting the dynamic balance between proinflammatory and proinflammatory cytokines.