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坏死性凋亡在大鼠蛛网膜下腔出血后早期脑损伤中的作用
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Journal Article
坏死性凋亡在大鼠蛛网膜下腔出血后早期脑损伤中的作用
2013
Overview
目的明确蛛网膜下腔出血（SAH）早期脑损伤中坏死性凋亡（necroptosis）通路的激活，探讨坏死性凋亡在SAH后早期脑损伤中的作用及其分子机制。方法40只雄性SD大鼠随机分为假手术组、SAH组、Nec1干预组、赋形剂组，血管内穿刺法建立SAH模型，干预组术前30min侧脑室注射坏死性凋亡的抑制剂Nec-1或赋形剂。各组于预定时间点评估神经功能，干湿重法测定脑组织含水量，碘化丙啶（PI）荧光法检测细胞坏死，免疫组化检测受体相互作用蛋白3（RIP3）的表达。结果与假手术组比较，SAH后RIP3的表达升高，并出现核移位，脑含水量及神经功能缺损加重，皮质及海马PI阳性细胞亦显著增加（P〈O．01）。给予Nee-1后RIP3表达水平较SAH组降低，同时脑组织内坏死的神经细胞及脑组织含水量减低，神经功能得到改善（P〈0．01）。结论坏死性凋亡在SAH后早期脑损伤中被激活并在神经功能损伤及脑水肿中发挥重要作用，RIP3可能作为坏死性凋亡通路的关键分子参与其中。抑制坏死性凋亡对SAH后早期脑保护及减轻脑水肿有蚕要意义。
