中华地方病学杂志
中華地方病學雜誌
중화지방병학잡지
Chinese Journal of Endemiology
2013年
6期
625-628
,共4页
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
氟中毒,牙%晚期糖基化終末產物受體%細胞覈因子κB%大鼠%海馬
불중독,아%만기당기화종말산물수체%세포핵인자κB%대서%해마
Fluorosis,Dental%Receptor for advanced glycation endproducts%Nuclear factor κB%Rats%Hippocampus
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κB(nuclear factor κB,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 ～ 120 g;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、50 mg/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±0.08,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.
目的 研究慢性氟中毒大鼠腦組織海馬中晚期糖基化終末產物受體(receptor for advanced glycation endproducts,RAGE)和細胞覈因子κB(nuclear factor κB,NF-κB)的錶達變化,探討氟中毒神經損害的髮病機製.方法 SD清潔級大鼠60隻,體質量為100 ～ 120 g;按體質量分為3組(每組20隻,雌雄各半),分彆為對照組、小劑量染氟組、大劑量染氟組,飲水含氟(氟化鈉,NaF)量分彆為＜0.5、10、50 mg/L;染氟6箇月後,經股動脈放血處死大鼠,取大鼠腦組織海馬,採用蛋白印跡方法和實時熒光定量PCR方法檢測RAGE和NF-κB蛋白、mRNA錶達.結果 與對照組[(100.00±2.60)％、(100.00±7.80)％]比較,小劑量染氟組、大劑量染氟組大鼠腦組織海馬中RAGE[(205.00±15.30)％、(232.00±10.90)％]和NF-κB[(156.00±12.20)％、(162.00±9.80)％]蛋白錶達均明顯升高(P均＜0.05);小劑量染氟組、大劑量染氟組大鼠腦組織海馬中RAGE(1.27±0.09、2.60±0.19)和NF-κB(0.83±0.15、1.27±0.19)mRNA錶達均高于對照組(0.66±0.18、0.32±0.08,P均＜0.05).結論 慢性氟中毒引起大鼠腦組織海馬中RAGE和NF-κB錶達明顯升高,這些改變可能與氟中毒性神經損傷髮生機製有一定的關繫.
목적 연구만성불중독대서뇌조직해마중만기당기화종말산물수체(receptor for advanced glycation endproducts,RAGE)화세포핵인자κB(nuclear factor κB,NF-κB)적표체변화,탐토불중독신경손해적발병궤제.방법 SD청길급대서60지,체질량위100 ～ 120 g;안체질량분위3조(매조20지,자웅각반),분별위대조조、소제량염불조、대제량염불조,음수함불(불화납,NaF)량분별위＜0.5、10、50 mg/L;염불6개월후,경고동맥방혈처사대서,취대서뇌조직해마,채용단백인적방법화실시형광정량PCR방법검측RAGE화NF-κB단백、mRNA표체.결과 여대조조[(100.00±2.60)％、(100.00±7.80)％]비교,소제량염불조、대제량염불조대서뇌조직해마중RAGE[(205.00±15.30)％、(232.00±10.90)％]화NF-κB[(156.00±12.20)％、(162.00±9.80)％]단백표체균명현승고(P균＜0.05);소제량염불조、대제량염불조대서뇌조직해마중RAGE(1.27±0.09、2.60±0.19)화NF-κB(0.83±0.15、1.27±0.19)mRNA표체균고우대조조(0.66±0.18、0.32±0.08,P균＜0.05).결론 만성불중독인기대서뇌조직해마중RAGE화NF-κB표체명현승고,저사개변가능여불중독성신경손상발생궤제유일정적관계.
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 ＜ 0.05]; 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.
