摘要
目的:研究慢性氟中毒大鼠大脑皮质中晚期糖基化终末产物(AGEs)及其受体(RAGE)表达,探讨氟中毒神经损害的发病机制。方法:60只SD大鼠按体质量随机分为对照组、小剂量染氟组和大剂量染氟组,采用酶联免疫方法、蛋白印迹方法和实时荧光定量PCR方法分别检测AGEs含量、RAGE的蛋白和mRNA表达水平。结果:染氟大鼠大脑皮质中AGEs含量和RAGE蛋白表达水平比对照组明显增高(P<0.05),染氟大鼠大脑皮质中RAGE的mRNA表达较对照组明显升高(P<0.05)。结论:慢性氟中毒引起大鼠大脑皮质中AGEs含量和RAGE表达明显升高,这些改变可能与氟中毒性神经损伤发生机制有关。
Objective： To investigate the expression changes of advanced glycation end products （AGEs） and receptor for advanced glyeation end products （RAGE） in brain cortex of rats with chronic fluorosis, and to study the mechanism of nerve damages caused by chronic fluorosis. Methods： The SD rats were randomly divided into control group （ group C）, small dosage of fluoride exposure group （group S） and large dosage of fluoride exposure group （group L）. The protein levels of AGEs and RAGE in the brain cortex of rats were detected with ELISA and Western blotting, and RAGE mRNA level were determined with quantitative real time PCR method. Results： The protein expression levels of AGEs and RAGE and the mRNA level of RAGE in the brain cortex of rats in group S and group L were significantly higher than those in group C. Conclusion： Chronic fluorosis can increase the expres- sions of AGEs and RAGE in the brain cortex of rats, which might be involved in brain damage.
出处
《贵阳医学院学报》
CAS
2013年第6期598-600,615,共4页
Journal of Guiyang Medical College
基金
国家自然科学基金(81160335)
科技部支撑计划课题(2013BAI05103)
科技部国际合作项目(2010DFB30530)
贵州省科学技术基金项目(2012)2040号
贵州省科技厅项目[(2011)7014号]
