二氧化氮与缺血性脑中风和血管性痴呆的相关性研究

Study on the correlation between nitrogen dioxide and ischemic stroke as well as vascular dementia

目的探讨二氧化氮与缺血性脑中风和血管性痴呆的发生发展的关系。方法制作MCAO大鼠模型,并进行NO2染毒,全自动血液流变仪检测NO2对大鼠血液流变学的影响,进行MCAO大鼠神经功能评分,检测NO2对MCAO大鼠神经功能恢复的影响;利用Western blot法检测大鼠大脑皮层中相关细胞因子。结果 NO2短期和长期暴露影响大鼠血液的血浆黏度,染毒组高于对照组(P<0.05);NO2长期暴露影响大鼠血液红细胞聚集指数,染毒组高于对照组(P<0.05);MCAO模型大鼠缺血再灌注3 d和5 d时,Stroke+NO2组大鼠神经功能和Stroke组比较有显著差别(P<0.05);NO2暴露后大鼠大脑皮层的ET-1表达增加,并且随着NO2暴露浓度的增加而增高;而e NOS、n NOS的表达量减少,并且随着NO2暴露浓度的增加而减少。结论 NO2污染与缺血性脑中风和血管性痴呆发生发展密切相关。

Objective To explore the occurrence and development relationship between nitrogen dioxide and isehemic stroke and vascular dementia. Methods The rat model of MCAO rats were established and automatic blood rheometer was used to test effect of NO2 on hemorheology in rats, neural function score in MCAO rats was carried out, and the effect of NO2 on neural function recovery of MCAO rats was studied. The related cytokines by Western blot assay in the rat cerebral cortex was tested. Results NO2 short term and long term exposure can affect blood plasma viscosity in rats, the exposure group was higher than that in the control group （ P 〈 0.05 ）. NO2 chronic exposure affected of red blood cell aggregation index of rats, exposure group was higher than control group （P 〈 0.05）. Ischemia reperfusion for 3 days and 5 days in MCAO models, there was significant difference in rat nerve function between Stroke ＋ NO2 group and stroke group （P 〈0.05）. The expression of ET-1 in cerebral cortex after exposure of NO2 was increased, and it increased with increasing of NO2 exposure concentrations, and eNOS, nNOS expression decreased, and it decreased with increasing of NO2 exposure concentration. Conclusion NO2 pollution is closely related to ischemic stroke and vascular dementia.