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目的:考察9-(4-乙氧羰基苯氧基)-6,7-二甲氧基-1,2,3,4-四氢吖啶盐酸盐(EDT)对大鼠局灶性脑缺血及谷氨酸(Glu)和硝普钠(SNP)致鼠皮层神经元损伤的作用。方法:灼断小鼠一侧大脑中动脉形成局灶性脑缺血模型,用氯化三苯基四氮唑(TTC)染色法测定脑梗塞率同时对神经症状进行评分。在原代培养的大鼠皮层神经细胞,采用MTT比色法,测定培养质内LDH及NO释放量。结果:EDT 2.5、5和10mg/kg及尼莫地平2mg/kg灌胃5d显著改善局灶性脑缺血小鼠的神经运动功能,缩小脑梗塞范围。在原代培养的鼠皮层神经细胞,EDT 0.01-3μmol/L浓度依赖地对抗Glu诱发的NO过量形成,并提高MTT微量比色值,同时,减少SNP引起的LDH过量释放,提高细胞存活率。结论:EDT能有效对抗脑缺血损伤,其神经保护作用可能是通过阻断Glu受体及抑制NO生成而实现的。
AIM: To investigate the effects of 9- (4-ethoxycarbonylphenoxy) -6,7-dimethoxy-1,2,3,4-tetrahydro acridine hydrochloride (EDT) on focal brain in rats Effects of ischemia and glutamate (Glu) and sodium nitroprusside (SNP) on neuronal damage in rat cortical. Methods: The model of focal cerebral ischemia was established by burning the middle cerebral artery of the mouse side. The cerebral infarction rate was measured by the method of triphenyltetrazolium chloride (TTC) staining and the neurological symptoms were scored. In primary cultured rat cortical neurons, MTT colorimetric method was used to determine the release of LDH and NO in culture media. RESULTS: EDT 2.5, 5 and 10 mg / kg and nimodipine 2 mg / kg for 5 days significantly reduced the neurological function and decreased the range of cerebral infarction in focal cerebral ischemia mice. In primary cultured rat cortical neurons, EDT 0.01-3μmol / L dose-dependently antagonized Glu-induced NO excess formation and increased MTT trace colorimetric values, meanwhile, it also reduced SNP overproduction of LDH and increased cell viability. Conclusion: EDT can effectively prevent cerebral ischemia injury and its neuroprotective effect may be through blocking Glu receptor and inhibiting NO production.