[1]雷波,谢宗义,马颖,等.大鼠蛛网膜下腔出血后皮质中VDAC1的表达与神经元凋亡的关系[J].陆军军医大学学报(原第三军医大学学报),2011,33(16):1705-1709.
　Lei Bo,Xie Zongyi,Ma Ying,et al.Correlation between VDAC1 expression and neuronal apoptosis in cerebral cortex of rats in early brain injury after subarachnoid hemorrhage[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(16):1705-1709.
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陆军军医大学学报（原第三军医大学学报）[ISSN:1000-5404/CN:51-1095/R]

卷:
33卷
期数:
2011年第16期
页码:
1705-1709
栏目:
论著
出版日期:
2011-08-30

文章信息/Info

Title:
Correlation between VDAC1 expression and neuronal apoptosis in cerebral cortex of rats in early brain injury after subarachnoid hemorrhage
作者:
雷波; 谢宗义; 马颖; 程远
重庆医科大学附属第二医院神经外科
Author(s):
Lei Bo;  Xie Zongyi;  Ma Ying;  Cheng Yuan
Department of Neurosurgery, Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400010, China
关键词:
蛛网膜下腔出血; 早期脑损伤; 细胞凋亡; VDAC1
Keywords:
subarachnoid hemorrhage;  early brain injury;  apoptosis;  VDAC1
分类号:
R743.35;R741.02
文献标志码:
A
摘要:
目的     观察大鼠蛛网膜下腔出血(subarachnoid hemorrhage, SAH)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，探讨电压依赖性阴离子通道蛋白1 (voltage-dependent anion channel1, VDAC1)参与SAH后早期脑损伤的发生机制。     方法     将SD大鼠108只按随机数字表法分为假手术组(n=18只)和SAH 组(n=90，下设SAH后6、12、36、48、72 h 5个时相点，每个时相点18只)。采用视交叉前池注血法建立SAH模型，应用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。     结果     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[mRNA(2.40±0.19)，蛋白(1.14±0.08)]，于36 h时表达达最高峰[mRNA(3.40±0.65)，蛋白(1.72±0.22)]，于48 h开始下降[mRNA(1.94±0.30)，蛋白(0.97±0.07)]，至72 h时基本恢复正常(P>0.05)。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)。     结论     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。
Abstract:
Objective     To study the correlation between voltage-dependent anion channel 1 (VDAC1) expression and neuronal apoptosis in the cerebral cortex of rats after subarachnoid hemorrhage (SAH), and to investigate the mechanism of VDAC1 involved in the early brain injury after SAH.      Methods     A total of 108 SD rats were randomly divided into a sham operation group (n=18) and an SAH group (n=90). The SAH group was subdivided into 6-, 12-, 36-, 48-, and 72-h subgroups (n=18 for each subgroup; 6, 12, 36, 48, and 72 hours after SAH, respectively). An SAH model was induced by injecting blood (300 μl) into the pre-chiasmatic cistern. VDAC1 expression in the cerebral cortex at both mRNA and protein levels were examined by RT-PCR as well as immunohistochemistry and Western blotting at 6, 12, 36, 48 and 72 h after SAH. Neuronal apoptosis in the cerebral cortex was evaluated by TUNEL at 6, 12, 36, 48 and 72 h after SAH.      Results     VDAC1 expression increased significantly at 12 h after SAH [mRNA (2.40±0.19), protein (1.14±0.08)], peaked at 36 h [mRNA (3.40±0.65), protein (1.72±0.22)], decreased at 48 h [mRNA (1.94±0.30), protein (0.97±0.07)], and fell to a normal level at 72 h (P>0.05). The number of apoptotic neurons in the cerebral cortex, as measured by TUNEL, increased at 12 h after SAH, reached the peak level at 36 h, then began to decrease (P<0.05), and fell to a normal level at 72 h (P>0.05).      Conclusion     There is a positive correlation between VDAC1 expression level and neuron apoptosis degree in the cerebral cortex of rats at different time points after SAH, implying that VDAC1 may be involved in the pathologic process of early brain injury after SAH through apoptotic pathways.

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更新日期/Last Update: 2011-08-30