摘要
目的:观察蛋白激酶C(PKC)选择性抑制剂灯盏花素乙(CH)对甲醛炎性痛时大鼠自发痛反应、脊髓一氧化氮合酶(NOS)表达和一氧化氮(NO)含量的影响,探讨炎性痛时脊髓内NO产生是否受PKC调控。方法:采用右后掌足底注射甲醛复制炎性痛模型;计数缩足反射次数反映自发痛程度;应用NADPH-d组织化学法测定脊髓NOS表达;硝酸/亚硝酸还原法测定脊髓腰膨大部位NO2-/NO3-含量。结果:甲醛炎性痛大鼠L5脊髓后角浅层和中央管周围灰质NADPH-d阳性细胞的数目、阳性细胞胞体及纤维的染色深度均明显大于正常对照组,脊髓腰膨大部位NO2-/NO3-含量明显增高。预先鞘内给予CH,可明显抑制甲醛炎性痛诱导的大鼠第二相自发痛反应以及脊髓NOS表达和NO2-/NO3-的含量。结论:炎性痛时,脊髓伤害性感受神经元内PKC激活可以促进NOS表达和NO的产生。
AIM： To study the effects of protein kinase C （PKC） inhibitor, cbelerythrine chloride （CH）, on nncicepfive response, nitric oxide synthase （NOS） expression and nitric oxide （NO） content in spinal cord of rats with inflammatory pain. METHODS： Inflammatory pain was induced by formalin injection into right hind paw. NADPH- d histochemistry was used to investigate the changes of NOS expression. Nitrate/nitrite （NO2^-/NO3^- ） was assayed to represent NO content.RESULTS： Compared with the control group, the number of NADPH - d positive cells increased significantly in the superficial layer （Laminae Ⅰ - Ⅱ ） of the spinal cord dorsal horn and the grey matter surrounding the central canal （laminae X ） in rats with inflammatory pain, the reactive degree of NADPH- d positive soma and fibers and NO content of the lumbar enlargement of spinal cord also increased significantly. Intrathecal injection of CH inhibited the spontaneous pain response in the second phase induced by formalin injection, and prevented the increases in the number and reactive degree of NADPH - d positive cells, as well as NO content of the lumbar enlargement of spinal cord. CONCLUSION： h is suggested that the activation of PKC promotes NOS expression and NO prnduction in the nnciceptive neurons of spinal cord during formalin- induced inflammatory pain.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2006年第3期532-536,共5页
Chinese Journal of Pathophysiology
基金
河北省自然科学基金资助项目(No.98276196D)
关键词
蛋白激酶C
一氧化氮
灯盏花素乙
甲醛
疼痛
脊髓
Protein kinase C
Nitric oxide
Chelerythrine chloride
Formaldehyde
Pain
Spinal cord
