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OALib Journal期刊
ISSN: 2333-9721
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低浓度so2暴露诱导大鼠大脑皮层的炎症效应
DOI: 10.3724/SP.J.1145.2014.09011, PP. 372-376
Keywords: 二氧化硫,大脑皮层,胶质细胞,炎症因子,胞外信号调节激酶,环磷腺苷效应元件结合蛋白
Abstract:
为了解低浓度二氧化硫（so2）慢性暴露对神经系统炎症反应的影响，通过建立wistar大鼠so2动式吸入染毒模型，采用荧光免疫组织化学方法考察低浓度so2（3.5和7mg/m3）慢性暴露下大鼠大脑皮层胶质细胞的活化反应，通过实时荧光定量pcr方法考察炎性因子的基因转录水平，并通过蛋白免疫印迹westernblot方法初步考察对与神经功能相关的胞外信号调节激酶亚型1和2（extracellularlyregulatedkinase1/2，erk1/2）及核转录因子环磷腺苷效应元件结合蛋白（campresponseelement-bindingprotein，creb）信号途径的影响.结果显示，长期低浓度so2暴露增加大脑皮层星形胶质细胞和小胶质细胞的活化反应，最高暴露组分别为对照组的2.07倍和2.12倍；诱导大鼠大脑皮层中促炎症因子tnfα和il-1β的mrna水平上调，最高暴露组分别为对照组的1.68和1.58倍；同时大鼠大脑皮层中诱导型环氧化酶（cyclooxygenase-2，cox-2）和诱导型一氧化氮合酶（induciblenitricoxidesynthase，inos）的mrna表达水平也明显增加，最高暴露组分别为对照组的1.59和1.45倍.此外，so2暴露组大鼠大脑皮层中p-creb和p-erk1/2的蛋白表达减少，最高暴露组分别为对照组的0.73和0.74倍.本研究表明，慢性低浓度so2暴露通过增加大鼠大脑皮层星形胶质细胞和小胶质细胞的活化反应，引起炎症因子tnfα、il-1β、inos和cox-2mrna的高表达，而且会引起p-erk1/2和p-creb的蛋白表达水平下调，提示so2暴露会通过炎症反应引起细胞信号传导和核转录的异常，导致神经功能损伤.
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