氟对大鼠脑组织α7尼古丁受体和ERK1/2影响  

Changes of alpha 7 nicotinic receptor and ERK1/2 in brain of rat with chronic fluorosis

作　　者：刘艳洁[1] 高勤[1] 吴昌学[2] 官志忠[1,2] 

机构地区：[1]贵阳医学院病理教研室,贵州贵阳550004 [2]贵阳医学院分子生物学实验室

出　　处：《中国公共卫生》2010年第10期1273-1274,共2页Chinese Journal of Public Health

基　　金：国家自然科学基金(30760224);科技部国际合作项目(2010DFB30530);贵州省省长资金项目[黔省专合字(2009)80号];高层次人才特助项目(TZJF-2008-53号)

摘　　要：目的研究氟对α7神经型尼古丁受体和细胞外信号调节蛋白激酶(ERK1/2)通路的影响。方法 SD大鼠随机分为3组,即对照组、低剂量染氟组、高剂量染氟组;实验6个月后,取大鼠脑组织,用蛋白印迹方法及实时荧光定量PCR方法分别检测尼古丁受体α7亚单位、ERK1/2激酶蛋白和mRNA表达。结果染氟大鼠脑组织中尼古丁受体α7亚单位蛋白表达降低[对照组(100±11.45)%,低剂量染氟组(45.2±9.2)%,高剂量染氟组(29.6±7.6)%];phospho-ERK1/2和total-ERK1/2蛋白表达升高[对照组(100.0±9.6)%、(100.0±11.7)%,低剂量染氟组(125.4±9.6)%、(132.9±2.1)%,高剂量染氟组(175.3±12.4)%、(207.4±7.4)%];染氟组ERK1/2活化率降低[对照组(100.0±12.2)%,低剂量染氟组(82.9±4.9)%,高剂量染氟组(65.9±3.7)%];染氟组尼古丁受体α7亚单位和ERK1/2 mRNA表达水平无明显改变;ERK1/2活化率与尼古丁受体α7亚单位蛋白表达呈正相关(r=0.696,P<0.05)。结论慢性氟中毒引起的脑组织ERK1/2信号通路改变可能与神经型尼古丁受体表达水平降低有关。Objective To investigate the expression of nicotinic acetylcholine receptors（nAChRs） and ERK1/2 pathway in the brain of rat with chronic fluorosis.Methods The SD rats were fed with different concentrations of fluoride（NaF） for six months to establish rat model with fluorosis.The protein levels of nAChR α7 subunit,extracellular signal-regulated protein kinase（ERK1/2） in rat brain were detected with Western-blotting and the mRNA level with quantitative real-time PCR.Results Compared to the control,in the rats treated with high concentrations of fluoride,the protein levels of nAChR α7 were significantly decreased（control：100%±11.5%;lower concentration group：45.2%±9.2%,higher concentration group：29.6%±7.6%）.Increased expression of phospho-ERK1/2 and total ERK1/2 at protein level were observed（control：100.0%±9.6% and 100.0%±11.7%,lower concentration group：125.4%±9.6% and 132.9%±2.1%,higher concentration group：175.3%±12.4 and 207.4%±7.4%）.However,the activation rate of ERK1/2 was lower in the brain of rats with fluorosis（control：100.0%±12.2%;lower concentration group：82.9.9%±4.9%;higher concentration group：65.9%±3.7%）.There was no difference of nAChR α7 subunit and ERK1/2 at mRNA level between the rats with fluorosis and controls.The decreased expression in nAChR α7 subunit had a correlation with the activation rate of ERK1/2（r=0.696,P0.05）.Conclusion The changed ERK 1/2 in brain induced by chronic fluorosis might be connected with the depressed expression of nAChR α7.

关 键 词：氟 神经型尼古丁受体 α7亚单位 ERK1/2 大鼠 

分 类 号：R599.9[医药卫生—内科学]