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目的:观察缺血后处理对大鼠局灶性脑缺血再灌注损伤后TLR4通路表达的影响。方法:成年健康雄性SD大鼠110只,随机分为假手术组(sham组)(n=10)、缺血再灌注组(I/R组)和后处理组(IP组),后两组又依据缺血再灌注6h、12h、24h、48h、72h不同的时间点再分五个亚组。对各组行神经行为学评分,脑组织梗死体积测量,TUNEL技术检测神经细胞凋亡的情况,免疫组织化学技术观察各组大鼠脑组织TLR4、NF-κB和TNF-α蛋白的表达,原位杂交方法检测各组大鼠脑组织TLR4mRNA、NF-κBmRNA的表达。结果:缺血后处理可下调TLR4、NF-κB、TNF-α细胞炎性因子的表达,抑制细胞凋亡、减少脑梗死体积,改善神经行为。结论:后处理可通过抑制TLR4信号通路表达,减少脑梗死体积,改善神经功能。
Objective: To observe the effect of ischemic postconditioning on TLR4 pathway after focal cerebral ischemia-reperfusion injury in rats. Methods: A total of 110 adult male Sprague-Dawley rats were randomly divided into sham group (n = 10), ischemia reperfusion group (I / R group) and postconditioning group (IP group) Again according to ischemia reperfusion 6h, 12h, 24h, 48h, 72h at different time points subdivided into five subgroups. Neurobehavioral score, infarct volume measurement and TUNEL technique were used to detect the neuronal apoptosis in each group. The expression of TLR4, NF-κB and TNF-α in brain tissue of each group were observed by immunohistochemistry Bit hybridization method to detect the expression of TLR4mRNA and NF-κBmRNA in the brain tissue of each group. Results: Ischemic postconditioning can down-regulate the expression of inflammatory factors of TLR4, NF-κB and TNF-α, inhibit apoptosis, decrease the volume of cerebral infarction and improve neurological behavior. Conclusion: Postconditioning can reduce the volume of cerebral infarction and improve neurological function by inhibiting the expression of TLR4 signaling pathway.