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首页> 外文期刊>Advances in Bioscience and Biotechnology >Chronic exposure to low doses of ozone produces a state of oxidative stress and blood-brain barrier damage in the hippocampus of rat
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Chronic exposure to low doses of ozone produces a state of oxidative stress and blood-brain barrier damage in the hippocampus of rat

机译:长期暴露于低剂量的臭氧会在大鼠海马中产生氧化应激和血脑屏障损害状态

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摘要

Chronic exposure to low doses of ozone similar to a day of high pollution in Mexico City causes a state of oxidative stress. This produces a progressive neurodegeneration in hippocampus of rats exposed to the gas. The aim of this study was to analyze the effect of chronic exposure on the changes in the blood-brain barrier in rats exposed to low doses of ozone. Method: each group received one of the following treatments, control group received air without ozone, and groups 2, 3, 4, 5, and 6 received ozone doses of 0.25 ppm for 4 h daily during 7, 15, 30, 60 and 90 days respectively. Each group was processed to inmunohistochemical technique against of the following antibody: blood-brain barrier, guanylyl cyclase, Iba-1, GFAP, NFκ-B, TNF-α. The results show that there is a correlation between the time exposure of ozone and the progressive damage, on the blood-brain barrier rupture, finally causing edema of endothelial cell, increase in guanylyl cyclase type 1, thickening of the processes and astrocytes foot, and an increase in the expression of factors NFκ-B and TNF-α at 30 and 60 days of exposure to this gas. All the above indicates that the chronic state of oxidative stress causes a neurodegeneration process, accompanied by disruption of the blood-brain barrier likely to occur in the Alzheimer’s disease.?
机译:慢性暴露于低剂量的臭氧中,类似于墨西哥城一天的高污染,导致氧化应激状态。这会在暴露于气体的大鼠海马中产生进行性神经变性。这项研究的目的是分析长期暴露对暴露于低剂量臭氧的大鼠血脑屏障变化的影响。方法:每组接受以下一种治疗,对照组接受无臭氧的空气,第2、3、4、5和6组在7、15、30、60和90期间每天接受0.25 ppm的臭氧剂量,持续4 h天分别。将各组针对以下抗体的免疫组织化学技术进行处理:血脑屏障,鸟苷酸环化酶,Iba-1,GFAP,NFκB,TNF-α。结果表明,臭氧暴露的时间与血脑屏障破裂上的进行性损害之间存在相关性,最终导致内皮细胞水肿,鸟嘌呤环化酶1型增加,突起和星形胶质细胞足增厚,以及在暴露于这种气体的30天和60天时,NFκB和TNF-α因子的表达增加。以上所有这些表明氧化应激的慢性状态会导致神经变性过程,并伴随着阿尔茨海默氏病中可能发生的血脑屏障破坏。

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