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Studies of the Molecular Mechanisms in the Development and Progression of Ischemic Stroke Induced by SO2 Inhalation

Author: HouLi
Tutor: SangZuo
School: Shanxi University
Course: Environmental Science
Keywords: Air pollution Sulfur dioxide SO2 Ischemic stroke Endothelial dysfunction Inflammatory response
CLC: R743.3
Type: Master's thesis
Year: 2010
Downloads: 39
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Abstract


With the continuous progress of industrialization, atmospheric pollutants, long-term low-level exposure and health problems caused by the acute pollution events is particularly prominent, has been a serious threat to human health. A large number of epidemiological results show that air pollution and stroke, and its effects are the main pollutants including SO2, NOx, O3, CO, and particulate matter. Which, SO2 in coal as its main energy in developing countries as a major air pollutants, the health effects of concern, but the current domestic and international research mainly concentrated on its correlation with respiratory diseases, as for the other tissues of the body organs the presence or absence of toxic effects is often overlooked, to determine induced effects and molecular mechanisms of stroke onset is rarely reported in the experimental conditions. Therefore, the introduction of this subject, designed to make up the blank of this field of research, the establishment of this effect detection and risk assessment of biological markers, provide a theoretical basis for the clinical treatment of health protection and pollution events. The subject first smoked by acting gas exposure to different concentrations of SO2 exposure of normal adult male Wistar rats, followed by Real-time RT-PCR technology, Western-blot technique were investigated in cerebral cortex, heart and lung in ischemic stroke-related factor endothelin -1 (ET-1), inducible nitric oxide synthase (iNOS) and cyclooxygenase -2 (COX-2), intercellular adhesion molecule -1 (ICAM -1) mRNA and protein expression changes; on the basis of the above studies, the establishment of focal cerebral ischemia reperfusion model (MCAO) rat model of low concentrations of SO2 exposure, and the effects of the exposure before and after The model rat cerebral cortex endothelial shrink factor, inflammatory factor and apoptosis-related gene expression changes. The results show that normal rat cerebral cortex in ET-1, iNOS, COX-2, ICAM-1 mRNA and protein levels of exposure with the SO2 concentration increased and increased in a dose-dependent effect; heart, lung tissue inflammation factor TNF-α, IL-1β, iNOS, ICAM-1 mRNA expression also showed the same trend, suggesting that SO2 inhalation caused the cardiopulmonary system damage induced inflammatory response, triggered after the release of inflammatory factors from entering the brain through the blood circulation system and promote ischemic injury in the brain tissue. The model Experimental results show MCAO rat brain cortex ischemic focal cerebral cortex in ischemic stroke associated factor ET-1, iNOS, COX-2, ICAM-1 expression than the sham group were significantly higher trend, caspase-3 activation, and SO2 inhalation aggravate the injury effect, thus confirming the SO2 pollution is to promote the development of the molecular mechanism of ischemic stroke, endothelial dysfunction and inflammatory responses.

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CLC: > Medicine, health > Neurology and psychiatry > Neurology > Cerebrovascular disease > Acute cerebrovascular disease ( stroke)
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