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Triptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa B signaling pathway

机译:雷公藤甲素通过抑制核因子κB信号转导通路减轻大鼠脑缺血和再灌注损伤

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Abstract: Inflammation plays critical roles in the acute progression of the pathology of ischemic injury. Previous studies have shown that triptolide interferes with a number of pro-inflammatory mechanisms. In this study, we investigated whether triptolide has protective effects during acute cerebral ischemia/reperfusion (I/R) injury. Male Sprague Dawley rats received triptolide or vehicle at the onset of reperfusion following middle cerebral artery occlusion. Twenty-four hours after reperfusion, we evaluated neurological injuries, the expression of pro-inflammatory markers, and NF-κB activation. I/R rats treated with triptolide showed significantly better neurological deficit scores, decreased neural apoptosis, and reduced cerebral infarct volume and brain edema, and triptolide treatment suppressed the activation of NF-κB following I/R injury. Furthermore, the expression levels of pro-inflammatory cytokines at both the mRNA and protein levels were significantly decreased in rats receiving triptolide. These results indicate that the neuroprotective effects of triptolide during acute cerebral I/R injury are possibly related to the inhibition of both the NF-κB signaling pathway and inflammation.
机译:摘要:炎症在缺血性损伤的病理过程中起着至关重要的作用。先前的研究表明雷公藤甲素会干扰多种促炎机制。在这项研究中,我们调查了雷公藤甲素是否在急性脑缺血/再灌注(I / R)损伤期间具有保护作用。雄性Sprague Dawley大鼠在大脑中动脉闭塞后再灌注时接受雷公藤甲素或媒介物治疗。再灌注后二十四小时,我们评估了神经系统损伤,促炎性标志物的表达以及NF-κB的活化。雷公藤甲素处理的I / R大鼠表现出明显更好的神经功能缺损评分,减少的神经细胞凋亡,减少的脑梗死体积和脑水肿,雷公藤甲素治疗抑制了I / R损伤后NF-κB的活化。此外,在接受雷公藤内酯醇的大鼠中,促炎细胞因子在mRNA和蛋白水平上的表达水平均明显降低。这些结果表明雷公藤甲素在急性脑I / R损伤期间的神经保护作用可能与NF-κB信号通路和炎症的抑制有关。

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