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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Calpeptin Reduces Neurobehavioral Deficits and Neuronal Apoptosis Following Subarachnoid Hemorrhage in Rats
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Calpeptin Reduces Neurobehavioral Deficits and Neuronal Apoptosis Following Subarachnoid Hemorrhage in Rats

机译：钙蛋白在大鼠蛛网膜下腔出血后降低神经兽性缺陷和神经元凋亡

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BackgroundInhibition of calpain activity provides neuroprotection in multiple central nervous system injury, but the role and mechanism of calpain in subarachnoid hemorrhage (SAH) remain unclear. This study was undertaken to determine the effects of inhibition of calpain on neurological deficit and neuronal apoptosis following experimental SAH. MethodsThe endovascular perforation model of SAH was produced in male Sprague-Dawley rats. Rats were administered calpeptin 50 μg, intracerebroventricular injection, 30 minutes before induction of SAH. After 72 hours, the method of Evans blue dye extravasation and wet/dry method were used for determination of blood-brain barrier permeability and brain edema, Western blot analysis and immunohistological staining were used to evaluate neuronal apoptosis. ResultsThe intracellular Ca2+level and calpain activity was significantly elevated in basal cortex after SAH. Calpain inhibitor calpeptin reduces brain water content and Evans blue dye extravasation, improves neurobehavioral deficits after SAH. Importantly, calpeptin treatment significantly reduces activation of caspase-3, caspase-9, caspase-12 and poly ADP ribose polymerase?and the number of apoptotic neurons in basal cortex after SAH. ConclusionThe present study suggested that calpeptin is neuroprotective in early brain injury after SAH through antiapoptotic effect.
机译：Brosefught Calpain Activity在多种中枢神经系统损伤中提供神经保护作用，但Calpain在蛛网膜下腔出血（SAH）中的作用和机制仍然不清楚。本研究旨在确定钙PAIN抑制对实验性SAH后神经缺陷和神经元细胞凋亡的影响。方法在雄性Sprague-Dawley大鼠制作SAH的血管穿孔模型。将大鼠捕获50μg，颅内腔内注射，诱导SAH诱导前30分钟。 72小时后，埃文斯蓝染料外渗和湿润/干法的方法用于测定血脑屏障渗透性和脑水肿，Western印迹分析和免疫组织染色用于评估神经元细胞凋亡。结果，在SAH后基础皮质中，CA2 +水平和CALPAIN活性显着升高。 Calpain抑制剂Calpeptin降低了脑水含量和埃文斯蓝染料外渗，在SAH后改善了神经兽性缺陷。重要的是，Calpeptin治疗显着降低了Caspase-3，Caspase-9，Caspase-12和Poly ADP核糖聚合酶的激活α和SAH后基底皮质中的凋亡神经元数。结论本研究表明，Calpeptin通过抗曝气效应后SAH早期脑损伤是神经保护的。

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