血管性痴呆模型大鼠NOS、NO的表达

The expression of nitric oxide synthase and nitric oxide in vascular dementia rats

目的观察血管性痴呆大鼠血浆和海马组织一氧化氮合酶和一氧化氮表达情况,探讨血管性痴呆的发病机制。方法采用改良的四血管法[1](4-VO)制备大鼠VaD模型,Morris水迷宫检测大鼠学习记忆能力,生化酶法检测大鼠血浆和脑组织tNOS和iNOS的酶活性以及NO含量,Western-blot法检测海马组织NOS蛋白表达情况,并对1月组和2月组表达差异进行对比分析。结果与对照组相比,VaD模型组大鼠逃避潜伏期明显延长,第一次穿越平台时间延长,穿越平台次数减少(P<0.05);VaD模型大鼠血浆及海马组织tNOS、iNOS活性和NO的含量明显增高(P<0.05);VaD模型大鼠海马组织NOS蛋白表达明显增高(P<0.01)。模型1月组血浆及海马组织NOS活性和NO的含量比模型2月组表达增高。结论 NOS酶活升高及海马组织高表达NOS可能是VaD海马神经元受损、学习记忆环路破坏、大鼠认知功能下降的原因。

Objective To observe the expression of nitric oxide synthase and nitric oxide in plasma and hipp campus tissue of vascular dementia rats so as to explore the pathogenesis of vascular dementia. Methods A modified four vessels occlusion method （4-VO） was used for VaD model rats preparation ,the Morris water maze test was used to detect the learn- ing and memory ability in rats, then biochemical enzymatic detection was used to determine the tNOS and iNOS enzyme ac- tivity and NO content in plasma and hippocampus tissue of rats, finally the western-blot assay was used to determine the NOS protein expression in the hippocampus tissue in order to make a comparative analysis on the differential expression be- tween sham operation group and VaD modle group. Also compare and analyse the protein expression between 1 month and 2 month group. Results Compared with sham operation group,the VaD model rats had significantly prolonged escape laten- cies, prolonged 1 st crossing platforms, reduced number of crossing platforms （ P 〈 0.05 ）, VaD model rats had significantly higher tNOS, iNOS enzyme activity and NO content in plasma and hippocampus tissue（ P 〈 0.05 ） ;VaD model rats had sig- nificantly increased NOS protein expression in hippocampus tissue（P 〈 0.01 ）. The NOS activity and NO content in plasma and hippocampus of 1 month model group were higher than those in 2 month model group. Conclusion The increased NOS enzyme activity and increased NOS expression in hippocampus tissue may be due to declined cognitive function caused by VaD hippocampal neurological impairment and learning and memory circuit damage.