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Effects of Brain derived neurotrophic factor (BDNF) and assessment using MRI on experimentally spinal cord Injury

脑源性神经营养因子 (BDNF) 的影响及 MRI 对实验性脊髓损伤的评估

基本信息

批准号：
12671396
负责人：
MURAKAMI Masazumi
金额：
$ 2.5万
依托单位：
CHIBA UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2001
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12671396/
关键词：
spinal cord injury brain derived neurotrophic factor rat oligodendrocyte apoptosis MRI apoptosis

项目摘要

We evaluated the effect of brain-derived neurotrophic factor (BDNF) on apoptosis after spinal cord injury. A rat spinal cord injury model was produced by static load, and continuous intrathecal BDNF or vehicle infusion was carried out either immediately or 3 days after the injury. Apoptotic cells were examined by nuclear staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). After injury, typical apoptotic cells were observed. Double staining with TUNEL and specific cell markers revealed that soon after the injury the apoptotic cells at the injury site were neurons and microglia. One week after the injury, apoptotic oligodendrocytes but not apoptotic astrocytes were observed in the white matter rostral and caudal to the injury site, whereas few apoptotic cells were found in the gray matter. The immediate BDNF treatment significantly reduced the number of TUNEL-positive cells in the adjacent rostral site 1 and 2 weeks after the injury, and in the adjacent caudal site 3 days and 1 week after the injury, even though there was no significant difference between BDNF-treated and control rats at the injury site itself. In addition, similar anti-apoptotic effects were observed in these regions 1 week after injury in rats that received BDNF treatment from the third day after injury. These findings suggest that BDNF suppresses delayed apoptosis of oligodendrocytes after spinal cord injury, for which even injections started late are effective. BDNF administration may therefore be useful for the clinical treatment of spinal cord injury through the suppression of secondary events.

我们评估了脑源性神经营养因子（BDNF）对脊髓损伤后细胞凋亡的影响。通过静态负荷建立大鼠脊髓损伤模型，并在损伤后立即或3天进行连续鞘内BDNF或载体输注。凋亡细胞通过核染色和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）检测。损伤后可见典型的凋亡细胞。TUNEL和特异性细胞标记物双重染色显示，损伤后即刻，损伤部位的凋亡细胞为神经元和小胶质细胞。损伤后1周，在损伤部位的头侧和尾侧的白色物质中观察到凋亡的少突胶质细胞，但未观察到凋亡的星形胶质细胞，而在灰质中发现很少的凋亡细胞。立即BDNF治疗显着减少了TUNEL阳性细胞的数量在邻近的头端部位损伤后1周和2周，并在邻近的尾侧部位损伤后3天和1周，即使有BDNF治疗组和对照组大鼠在损伤部位本身没有显着差异。此外，在损伤后第三天接受BDNF治疗的大鼠中，在损伤后1周在这些区域观察到类似的抗凋亡作用。这些发现表明，BDNF抑制脊髓损伤后少突胶质细胞的延迟凋亡，即使注射开始较晚也有效。因此，BDNF给药可能有助于通过抑制继发性事件来临床治疗脊髓损伤。