戊四氮致痫大鼠海马一氧化氮的变化及对海马神经元凋亡的影响
The changes of hippocampal NO on pentylenetetrazol induced epileptic rats and its effect to hippocampal neuronal apoptosis
摘要目的 观察戊四氮(PTZ)致痫大鼠海马一氧化氮(NO)的变化对神经元兴奋毒性的影响.方法 SD雄性大鼠随机分为3组,每组14只,分别用生理盐水(A组)、PTZ(B组)、氨基胍+PTZ(C组)造模后,对海马NO含量、谷氨酸(Glu)免疫反应性、半胱氨酸酶(Caspase)-3 mRNA水平进行检测分析.结果 B组海马NO含量为(75.67±2.04) μmol/L,与A组(11.90±0.64) μmol/L和C组(36.19±4.48) μmol/L比较差异有统计学意义(P<0.05);A组和C组的Glu、caspase-3 mRNA 表达水平明显低于B组(P<0.05).结论 戊四氮致痫后可导致大鼠海马NO过量产生,对海马神经元具有兴奋毒性作用.而一氧化氮合成酶抑制剂的干预,具有神经保护作用.
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abstractsObjective To study the changes of nitric oxide (NO) content in hippocampus of rat by Pentylenetetrazol ( PTZ)-induced seizures models and its effect of toxicity and apoptosis.Methods SD male rats were random divided into three groups,each group has 14 rats.Group A is the saline control group,group B is the pentylenetetrazol induced epileptic group and group C is aminoguanidine ( NOS inhibitor) pretreatment plus pentylenetetrazol induced epileptic group.NO content in rat hippocampus was detected by ultraviolet spectrophotometry,glutamate ( Glu ) immunoreactivity in rat hippocampus was detected by immunohistochemistry (SABC) and caspase-3 mRNA levels in rat hippocampus were detected by reverse transcription-polymerase chain reaction (RT-PCR) respectively at 2,48 h after modeling.Results Group A had no seizure,group B had epilepsia gravior over Ⅴ grade,rats in group C had seizure over Ⅱ Ⅲ grade.The NO content on group B (75.67 ± 2.04) μ mol/L was significantly higher than group A (11.90±0.64) μmol/L and group C (36.19 ±4.48) μmol/L (P<0.05) ; Glu immunoreactivity and caspase-3 mRNA leves of group A and group C were lower than group B ( P < 0.05 ).Conclusion PTZinduced seizures may lead to excessive production of NO in hippocampus,which had excited toxicity to hippocampal neurons.The intervention of NOS synthetic inhibitor had neuroprotective effects.
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