Association between VDAC1 expression and neuronal apoptosis in the cerebral cortex in the early brai.docVIP
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Association between VDAC1 expression and neuronal apoptosis in the cerebral cortex in the early brai.doc
大鼠蛛网膜下腔出血后皮质中VDAC1的表达与神经元凋亡的相关性研究
雷 波,谢宗义,马 颖,程 远 (400010重庆,重庆医科大学附属第二医院神经外科)
[摘要] 目的:观察大鼠蛛网膜下腔出血(subarachnoid hemorrhageSAH)后大脑皮质中VDAC1表达和皮质神经元凋亡,以及两者之间的关系,探讨VDAC1参与SAH后早期脑损伤的发生机理。SD大鼠108只,随机分为假手术组和SAH 组6、12、36、48、72 h 5个。采用视交叉前池注血法建立SAH模型,应用逆转录聚合酶链反应RT-PCR)、免疫组化和Western Blot分别检测大鼠SAH后不同时相点VDAC1在mRNA水平、蛋白质水平的表达变化凋亡原位末端标记法(Tunel)观察SAH后不同时相点大脑皮质神经元凋亡。大脑皮质中VDAC1表达,无论在mRNA水平,还是在蛋白质水平,在SAH后12 h均明显增加RNA( ??).,蛋白(??)],于36h时表达达最高峰RNA( ??).,蛋白(??)],于48 h开始下降,至72 h时基本恢复正常( P 0. 01)。TUNEL法检测显示大鼠SAH后12 h,大脑皮质中神经元凋亡细胞数开始增加,36 h达到高峰,之后逐渐降低(P 0. 05),72 h时降至正常( P 0. 05)。SAH后不同时间点VDAC1表达水平的动态变化与神经元凋亡发生发展的时相性是一致的,提示VDAC1可能通过细胞凋亡途径参与SAH后早期脑损伤的病理过程。
关键词蛛网膜下腔出血;早期脑损伤;细胞凋亡;VDAC1
Association between VDAC1 expression and neuronal apoptosis in the cerebral cort in the early brain injury after subarachnoid hemorrhage in rats
Lei Bo, Xie Zongyi, Ma Ying, Cheng Yuan (Department of Neurosurgery, Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.)
[Abstract] Objective To observe the relation between VDAC1 expression and neuronal apoptosis in the cerebral cortex and investigate the mechanism of VDAC1 involved in the early brain injury after subarachnoid hemorrhage (SAH). Methods A total of 72 SD rats were randomly divided into the sham-operated group and SAH group. The SAH group was subdivided into 6, 12, 36, 48 and 72 hours subgroup after SAH. Experimental SAH model was induced by blood injection into the pre-chiasmatic cistern (300μL). The changes of VDAC1 expression in the cerebral cortex were examined by Reverse Transcriptase Polymerase Chain Reaction (RT-PCR), immunohistochemistry and Western Blot at different time points following SAH. The neuronal apoptosis in the cerebral cortex were measured at 6, 12, 36, 48 and 72 h by TUNEL. Results Expression of VDAC1 in the level of mRNA and protein in the cerebral cortex began to increase dramatically at 12 h after SAH, peaked at 36 h (P0.05), and significantly decreased at later observation times, finally nor
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