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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Exercise Preconditioning Regulates the Toll-Like Receptor 4/Nuclear Factor-kappa B Signaling Pathway and Reduces Cerebral Ischemia/Reperfusion Inflammatory Injury: A Study in Rats
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Exercise Preconditioning Regulates the Toll-Like Receptor 4/Nuclear Factor-kappa B Signaling Pathway and Reduces Cerebral Ischemia/Reperfusion Inflammatory Injury: A Study in Rats

机译:运动预处理可调节Toll样受体4 /核因子-κB信号通路并减少脑缺血/再灌注性炎症损伤:一项对大鼠的研究

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Objective: To explore the influence of exercise preconditioning (EP) on the activity of the toll-like receptor (TLR)4uclear factor (NF)-kappa B signaling pathway in a rat model of cerebral ischemia/reperfusion (I/R) inflammatory injury. Methods: Ischemia was induced in rats using transient middle cerebral artery occlusion (tMCAO) after 3 weeks of EP. Fifty-four rats were divided into sham, MCAO, and EP+MCAO groups. Following the induction of cerebral I/R injury, rats were scored for neurological deficits. Various techniques were used to evaluate ischemic infarct volume and explore pathological changes in tissue morphology after cerebral I/R injury, wherein the levels of TLR4 and NF-kappa B were analyzed. In addition, enzyme-linked immunosorbent assays were used to detect the levels of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta in peripheral serum. Results: Twenty-four hours after cerebral I/R injury, the neurological deficit scores decreased and ischemic cortical damage alleviated in EP+MCAO group; the number of TLR4- and NF-kappa B-positive cells, the expression of TLR4 and NF-kappa B in the ischemic side, and the concentrations of TNF-alpha and IL-1 beta in the peripheral serum were lower in EP+MCAO group than those in the MCAO group (P<.05). Conclusions: The present study indicates that EP can improve cerebral I/R-induced neurological deficits in rats, reduce infarct volume, mitigate pathological damage in the ischemic cortex, and exert neuroprotective effects. The mechanism underlying these effects might involve the regulation of the TLR4/NF-kappa B signaling pathway and the inhibition of central and peripheral inflammatory cascades during cerebral I/R injury.
机译:目的:探讨运动预适应(EP)对大鼠脑缺血/再灌注(I / R)模型中toll样受体(TLR)4 /核因子(NF)-κB信号通路活性的影响炎性损伤。方法:EP 3周后,采用短暂性大脑中动脉闭塞(tMCAO)诱导大鼠缺血。 54只大鼠分为假手术,MCAO和EP + MCAO组。诱发脑I / R损伤后,对大鼠进行神经功能缺损评分。多种技术被用于评估缺血性脑梗死体积并探讨脑I / R损伤后组织形态的病理变化,其中分析了TLR4和NF-κB的水平。另外,使用酶联免疫吸附试验检测外周血中肿瘤坏死因子(TNF)-α和白介素(IL)-1β的水平。结果:EP + MCAO组脑I / R损伤后24小时,神经功能缺损评分降低,缺血性皮层损伤减轻。 EP + MCAO中TLR4-和NF-κB阳性细胞数目,局部缺血侧TLR4和NF-κB的表达以及外周血清TNF-α和IL-1β的浓度较低与MCAO组相比(P <.05)。结论:本研究表明,EP可以改善脑I / R诱导的大鼠神经功能缺损,减少梗塞体积,减轻缺血皮层的病理损伤,并发挥神经保护作用。这些作用的潜在机制可能涉及TLR4 /NF-κB信号通路的调节以及对脑I / R损伤中中枢和外周炎症级联反应的抑制。

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