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一氧化氮:脊髓空洞症的一个可能病因

Nitric oxide: a possible etiologic factor in spinal cord cavitation.

作者信息

Matsuyama Y, Sato K, Kamiya M, Yano J, Iwata H, Isobe K

机构信息

Department of Orthopaedic Surgery, Nagoya University School of Medicine, Japan.

出版信息

J Spinal Disord. 1998 Jun;11(3):248-52.

PMID:9657552
Abstract

To determine whether nitric oxide (NO) is related to spinal cord cavitation, we treated mice that underwent spinal cord injury with NG-mono-methyl-L-arginine (N-MMA). Spinal cord specimens were subjected to glial fibrillary acidic protein (GFAP) immunostaining, which is selective for astrocytes. Spinal cord cavities and GFAP-positive glial cells appeared simultaneously at 3 days after spinal cord injury, and the cavities enlarged at 7 days. In mice receiving N-MMA, the cavities were significantly smaller than those in the mice that underwent spinal cord injury only. However, the numbers of GFAP-positive cells showed no difference between these two groups. These experimental findings suggest that cavitation of the spinal cord is caused mainly by NO released from activated glial cells.

摘要

为了确定一氧化氮(NO)是否与脊髓空洞症有关,我们用N-单甲基-L-精氨酸(N-MMA)处理脊髓损伤的小鼠。脊髓标本进行了胶质纤维酸性蛋白(GFAP)免疫染色,该染色对星形胶质细胞具有选择性。脊髓空洞和GFAP阳性胶质细胞在脊髓损伤后3天同时出现,且空洞在7天时扩大。在接受N-MMA的小鼠中,空洞明显小于仅接受脊髓损伤的小鼠。然而,这两组之间GFAP阳性细胞的数量没有差异。这些实验结果表明,脊髓空洞主要由活化胶质细胞释放的NO引起。

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