Sun Xiao-Cai, Chen Wei-Na, Li Shu-Qin, Cai Jin-Song, Li Wen-Bin, Xian Xiao-Hui, Hu Yu-Yan, Zhang Min, Li Qing-Jun
Department of Pathophysiology, Institute of Basic Medicine, Hebei Medical University, 361 Zhongshan East Road, Shijiazhuang, 050017, People's Republic of China.
Neurochem Res. 2009 Feb;34(2):351-9. doi: 10.1007/s11064-008-9785-7. Epub 2008 Jul 16.
Previous experiments have suggested that nitric oxide plays an important role in nociceptive transmission in the spinal cord. In order to explore the involvement of glia in the NO-mediated nociceptive transmission, the present study was undertaken to investigate the effect of fluorocitrate (FC), an inhibitor of glial metabolism, on NOS expression and activity and NO production in the spinal cord during the process of peripheral inflammatory pain and hyperalgesia induced by formalin test in rats. Sixty adult male Sprague-Dawley rats were randomly assigned into sham, formalin, formalin + normal saline (NS), and formalin + FC groups. The NOS expression, NOS activity and NO production was detected by NADPH-d histochemistry staining, NOS and NO assay kit, respectively. It was found that formalin test significantly up-regulated NOS expression and activity and NO production in the laminae I-II of the dorsal horn and the grey matter around the central canal in the lumbar spinal cord at 1 h after the formalin test. Selective inhibition of glia metabolism with intrathecal administration of FC (1 nmol) significantly inhibited the up-regulation in NOS expression and activity and NO production normally induced by the formalin test, which was represented with decreases in the number and density of the NADPH-d positive cells in the dorsal horn and grey matter around the central canal, and decrease in density of NADPH-d positive neuropil in the dorsal horn in formalin + FC group compared with formalin group. The results suggested that glia may be involved in the NO-mediated nociceptive transmission in the spinal cord.
先前的实验表明，一氧化氮在脊髓伤害性信息传递中起重要作用。为了探究胶质细胞在一氧化氮介导的伤害性信息传递中的作用，本研究旨在考察胶质细胞代谢抑制剂氟代柠檬酸（FC）对大鼠福尔马林试验诱导的外周炎性疼痛和痛觉过敏过程中脊髓一氧化氮合酶（NOS）表达、活性及一氧化氮（NO）生成的影响。将60只成年雄性Sprague-Dawley大鼠随机分为假手术组、福尔马林组、福尔马林+生理盐水（NS）组和福尔马林+FC组。分别采用NADPH-d组织化学染色、NOS和NO检测试剂盒检测NOS表达、NOS活性及NO生成。结果发现，福尔马林试验后1小时，福尔马林试验显著上调了腰段脊髓背角I-II层及中央管周围灰质中NOS的表达、活性及NO生成。鞘内注射FC（1 nmol）选择性抑制胶质细胞代谢，显著抑制了福尔马林试验正常诱导的NOS表达、活性及NO生成上调，表现为福尔马林+FC组与福尔马林组相比，背角及中央管周围灰质中NADPH-d阳性细胞数量和密度降低，背角NADPH-d阳性神经纤维密度降低。结果提示，胶质细胞可能参与脊髓中一氧化氮介导的伤害性信息传递。
