慢性氟中毒大鼠脑组织海马中晚期糖基化终末产物受体和细胞核因子κB的改变  

Expression of receptor for advanced glycation endproducts and nuclear factor κB in brain hippocampus of rat with chronic fluorosis

作　　者：张凯琳[1] 楼迪栋[1] 官志忠[1] 

机构地区：[1]贵阳医学院病理教研室,550004

出　　处：《中华地方病学杂志》2013年第6期625-628,共4页Chinese Journal of Endemiology

基　　金：国家自然科学基金（81160335）;国际科技合作项目（2010DFB30530）;科技部支撑计划（2011BAZ03220）;贵州省科学技术基金（黔科合J字[201212040号）;贵州省科技厅项目（黔科合外G字[2011]7014号）

摘　　要：目的研究慢性氟中毒大鼠脑组织海马中晚期糖基化终末产物受体（receptor for advanced glycation endproducts，RAGE）和细胞核因子KB（nuclearfactorKB，NF—κB）的表达变化，探讨氟中毒神经损害的发病机制。方法SD清洁级大鼠60只，体质量为100—120g；按体质量分为3组（每组20只，雌雄各半），分别为对照组、小剂量染氟组、大剂量染氟组，饮水含氟（氟化钠，NaF）量分别为〈0．5、10、50mg／L；染氟6个月后，经股动脉放血处死大鼠，取大鼠脑组织海马，采用蛋白印迹方法和实时荧光定量PCR方法检测RAGE和NF—κB蛋白、mRNA表达。结果与对照组[（100．00±2．60）％、（100．00±7．80）％]比较，小剂量染氟组、大剂量染氟组大鼠脑组织海马中RAGE[（205．00±15．30）％、（232．00±10．90）％]和NF—κB[（156．00±12．20）％、（162．00±9．80）％]蛋白表达均明显升高（P均〈0．05）；小剂量染氟组、大剂量染氟组大鼠脑组织海马中RAGE（1．27±0．09、2．60±0．19）和NF—κB（0．83±0．15、1．27±0．19）mRNA表达均高于对照组（0．66±0．18、0．32±O．08．P均〈0．05）。结论慢性氟中毒引起大鼠脑组织海马中RAGE和NF—κB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一定的关系。Objective To investigate the expressions of receptor for advanced glycation endproducts （RAGE） and nuclear factor κB （NF-κB） in brain hippocampus of rat with chronic fluorosis, and to reveal the mechanism of brain damage resulted from chronic fluorosis. Methods Sixty Clean grade SD rats were randomly divided to three groups（20 rats in each group, 10 female and 10 male） fed with different contents of fluoride, control group with normal tap-water（ 〈 0.5 mg/L fluoride）, small dosage of fluoride exposure group（ 10 mg/L fluoride in tap-water） and large dosage of fluoride exposure group （50 mg/L fluoride） for six months. Then the rats were killed by femoral artery bleeding and hippocampus was removed. Protein and mRNA levels of RAGE and NF-κB in the hippocampus were determined by Western blotting and quantitative real time PCR, respectively. Results As compared to the control groups[ （100.00 ± 2.60）%, （100.00 -± 7.80）%], the expressions of RAGE and NF-κB at protein level in the hippocampus were significantly increased in the small dosage of fluoride exposure groups [ （205.00 ± 15.30）%, （156.00 ± 12.20）%] and the large dosage of fluoride exposure groups[ （232.00 ± 10.90）%, （162.00 ± 9.80）%, all P 〈 0.057; for,the mRNA level of RAGE and NF-κB, the expressions were higher in the small dosage of fluoride exposure groups（1.27 ± 0.09, 0.83 ± 0.15） and the large dosage of fluoride exposure groups （2.60 ± 0.19, 1.27 ± 0.19） than those of the control groups（0.66 ± 0.18, 0.32 ± 0.08, all P 〈 0.05）. Conclusions The increased expressions of RAGE and NF-κB in the hippocampus of rat brain are caused by chronic fluorosis,and these changes may be associated with the mechanism of nerve injury.

关 键 词：氟中毒 牙 晚期糖基化终末产物受体 细胞核因子ΚB 大鼠 海马 

分 类 号：R595.1[医药卫生—内科学]