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作 者:舒勤奋[1] 刘小利[1] 金煜[1] 吴炯[1] 姜寿峰[1] 倪娇娜[1] 罗祖明[1]
出 处:《全科医学临床与教育》2008年第4期297-299,F0002,共4页Clinical Education of General Practice
摘 要:目的观察局灶性缺血预处理对大鼠肿瘤坏死因子(TNF-a)的表达影响,探讨TNF-a与缺血耐受的关系及其在内源性保护机制中的作用。方法利用线栓法建立局灶性脑缺血耐受的动物模型。选用30只SD大鼠,随机将30只大鼠分为实验组:预缺血+缺血(IP+MCAO);假手术组(SS+MCAO):假手术代替IP,余同实验组;对照组(SS+SS),每组10只。评价指标包括神经功能缺损评分、光镜下组织病理改变及免疫组织化学染色和图像分析比较各组TNF-a的表达变化。结果局灶性IP能够明显改善3d后的大鼠的神经功能评分,减轻组织学的损伤,下调了TNF-a的表达,IOD值实验组(8109.53±571.21)对比假手术组(10704.72±584.01),差异有统计学意义(F=233.59,P<0.05)。结论局灶性缺血预处理对随后的脑梗死有明显的保护作用,能够诱导缺血耐受的产生,其可能的机制是通过下调肿瘤坏死因子的表达。Objective To explore the effects of focal cerebral ischemic preconditioning on the expression of tumor necrosis factor-alpha and the relationship of tumor necrosis factor-alpha and ischemic tolerance. Methods The animal model of focal cerebral ischemic tolerance was used. 30 SD rats were divided into 3 groups : IPC+MCAO group, SS+MCAO group and SS+SS group. The infarct volume and histological changes with HE staining were evaluated .The expression of tumor necrosis factor-alpha was evaluated by immunohistochemistry. Results Focal cerebral ischemic preconditioning significantly reduced the following infarct volume and the damage of histology.The interagrated optical density in IPC+MCAO group and SS+MCAO group were (8109.53± 571.21 ) and (10704.72±584.01) respectively,which had statistic significance (F=233.59,P〈0.05). Conclusions Focal cerebral ischemic preconditioning can protect brain and induce ischemic tolerance. Down-regulation of the expression of tumor necrosis factor-alpha may play an important role in the induction of endogenous neuroprotection.
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