论文部分内容阅读
目的观察一氧化氮含量的变化对缺血再灌注损伤后Fos蛋白表达的影响。方法采用线拴法制作大鼠局灶性脑缺血再灌注损伤模型，利用NADPH组化和Fos蛋白免疫组化双标技术研究NOS抑制剂L－NAME对大鼠局灶性脑缺血再灌注损伤脑皮层Fos蛋白表达的影响。结果缺血60min再灌注3h后损伤侧脑组织皮质一氧化氮合酶阳性神经元较正常增多并深染，Fos蛋白表达增加，L－NAME（3mg／kg）治疗组脑皮质神经元Fos蛋白的表达量较对照组减少，L－NAME（10mg/kg）治疗组脑皮质神经元Fos蛋白的表达量较对照组明显减少，同时也可见给予L－NAME后脑组织皮质内NOS阳性神经元无论在数量上还是在细胞着色、胞体突起均明显减少。结论c－fos基因表达也可能部分参与了NO的致神经细胞损伤过程。
Objective To observe the effect of nitric oxide on Fos protein expression after ischemia-reperfusion injury. Methods Fetal focal cerebral ischemia-reperfusion injury model was made by tethering method. The effects of NOS inhibitor L-NAME on focal cerebral ischemia-reperfusion in rats were studied by NADPH staining and Fos protein immunohistochemistry Effect of Fos protein expression in injured cortex. Results The cortical nitric oxide synthase (NOS) -positive neurons in injured cortex at 60 min after ischemia were increased and stained darker than normal, and the expression of Fos protein was increased. The expression of Fos protein in cortical neurons of L-NAME (3 mg / kg) Compared with the control group, the expression of Fos protein in cerebral cortical neurons of L-NAME (10 mg / kg) group was significantly decreased compared with that of the control group, and NOS positive neurons in cortex of L-NAME group On or in the cell coloring, somatic cell protrusions were significantly reduced. Conclusions The expression of c-fos gene may be partially involved in the process of NO-induced neuronal injury.