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目的 为了研究 NO在局灶性脑缺血再灌流过程中对神经细胞的作用机制 ,特别是 NO与细胞凋亡的关系。方法 利用 RT- PCR方法观察了细胞凋亡相关基因 Bcl- x和 ICE在 NNL A干预后局灶性脑缺血鼠脑组织中的表达水平。结果 局灶性脑缺血再灌流模型中凋亡相关基因的检测结果显示 :(1) Bcl- x的表达在手术侧缺血期呈下降趋势 ,在再灌流期呈升高趋势 ;非手术侧改变不明显。 (2 )小剂量 NNL A具有抑制 Bcl- x表达的作用。(3) ICE的表达在缺血期表现为下降 ,而再灌流期则改变不明显 ;非手术侧均有升高趋势。结论 在局灶性脑缺血再灌流过程中 ,Bcl- x通过其表达量的增加 ,具有抑制细胞凋亡的作用。同时 Bcl- x还有可能通过抑制 ROS激活ICE的过程或直接抑制 ROS的生成达到抑制凋亡的作用 ,所以 ICE的表达水平下降则可能与 Bcl- x升高有关。NO在局灶性脑缺血再灌流过程中同时影响 Bcl- x和 ICE的表达 ,这种影响与其对病理改变的影响是一致的
Objective To study the mechanism of action of NO on nerve cells during focal cerebral ischemia and reperfusion, especially the relationship between NO and apoptosis. Methods The expression levels of Bcl-x and ICE in brain tissue after focal cerebral ischemia in NNL A-treated rats were observed by RT-PCR. Results The results of apoptosis-related genes in focal cerebral ischemia-reperfusion model showed that: (1) The expression of Bcl-x showed a decreasing trend in the ischemic period of the operation side and a rising trend in the reperfusion period; the non-operation side Change is not obvious. (2) Low dose NNL A can inhibit the expression of Bcl-x. (3) The expression of ICE decreased in ischemic phase, but not obvious in reperfusion phase. The non-surgical side showed an increasing trend. Conclusion During the process of focal cerebral ischemia-reperfusion, Bcl-x can inhibit the apoptosis through the increase of its expression. At the same time, Bcl-x may inhibit the activation of ICE by ROS or directly inhibit the production of ROS to inhibit apoptosis, so the decreased expression of ICE may be related to the increase of Bcl-x. NO also affects the expression of Bcl-x and ICE during focal cerebral ischemia / reperfusion, which is consistent with its effect on pathological changes