Although the effect of activated protein C (APC) on neuronal injury and neuroinflammatory responses has been extensively studied, the detailed mechanism underlying APC-protective effect in the blood-brain barrier (BBB) injury during ischemia is still not clear. In this study, the APC effect against neuroinflammatory responses was evaluated in the model of right middle cerebral artery occlusion in male Sprague-Dawley rats with 2 hours of ischemia and 22 hours of reperfusion. The results showed that APC can significantly improve the neurological function scoring and reduce the infarct volume and BBB permeability. Moreover, the expression of protein nuclear factor-kappa B (NF-κB), both in cytoplasm and nuclei, was reduced. The downstream of NF-κB activation, including tumor necrosis factor-α and interleukin-1β secretion, was inhibited. In all, APC exerts a neuroprotective effect in focal cerebral ischemia-reperfusion in rats by inhibiting the activation and nuclear translocation of NF-κB. It may indicate a therapeutic approach for ischemic brain injury.

中文翻译：

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活化蛋白C对局灶性脑缺血/再灌注期间血脑屏障损伤的神经保护作用。

尽管已经广泛研究了活化蛋白C（APC）对神经元损伤和神经炎症反应的作用，但尚不清楚缺血过程中APC保护作用在血脑屏障（BBB）损伤中的详细机制。在这项研究中，在雄性Sprague-Dawley大鼠缺血2小时和再灌注22小时的右大脑中动脉闭塞模型中评估了APC对神经炎症反应的作用。结果表明，APC可以显着改善神经功能评分，并减少梗死体积和BBB通透性。此外，蛋白质核因子-κB（NF-κB）在细胞质和细胞核中的表达均降低。抑制了NF-κB激活的下游，包括肿瘤坏死因子-α和白介素-1β的分泌。在所有，APC通过抑制NF-κB的活化和核易位，在大鼠局灶性脑缺血再灌注中发挥神经保护作用。它可能表明缺血性脑损伤的治疗方法。