中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2010年
1期
63-66
,共4页
张毅%张生林%高凤花%陈芸%杨晓娟
張毅%張生林%高鳳花%陳蕓%楊曉娟
장의%장생림%고봉화%진예%양효연
糖尿病%2型%阿尔茨海默病%糖原合成激酶3%氧化磷酸化
糖尿病%2型%阿爾茨海默病%糖原閤成激酶3%氧化燐痠化
당뇨병%2형%아이자해묵병%당원합성격매3%양화린산화
Diabetes mellitus%type 2%Alzheimer disease%Glycogen synthase kinase 3%Oxidative plosphorylation
目的 研究2型糖尿病(T2DM)并发阿尔茨海默病(AD)的可能机制. 方法 选取同龄Wistar大鼠,随机分为正常对照组、T2DM组、AD组及T2DM+AD组.采用血糖仪监测大鼠血糖,水迷宫实验观测大鼠行为学改变,免疫组化染色检测大鼠糖原合成激酶-3β(GSK-3β)及tau蛋白磷酸化水平. 结果 各模型组大鼠均较正常对照组学习记忆力减退,T2DM组与AD组及T2DM+AD组之间差异有统计学意义(F=28.65 P<0.001).T2DM+AD组GSK-3β表达水平(4319.02±653.24)显著高于T2DM组(540.43±558.49)、正常对照组(315.56±91.64)及AD组(304.39±175.83)(H=19.335,P<0.001).AD组(2799.61±1070.02)及T2DM+AD组(8583.814±2236.11)tau蛋白磷酸化表达水平显著高于正常对照组(252.024±58.37)及T2DM组(287.75±192.53)(H=32.950,P<0.001). 结论 T2DM大鼠GSK-3β活性的上调可能是引起大鼠tau蛋白磷酸化的一个重要原因.
目的 研究2型糖尿病(T2DM)併髮阿爾茨海默病(AD)的可能機製. 方法 選取同齡Wistar大鼠,隨機分為正常對照組、T2DM組、AD組及T2DM+AD組.採用血糖儀鑑測大鼠血糖,水迷宮實驗觀測大鼠行為學改變,免疫組化染色檢測大鼠糖原閤成激酶-3β(GSK-3β)及tau蛋白燐痠化水平. 結果 各模型組大鼠均較正常對照組學習記憶力減退,T2DM組與AD組及T2DM+AD組之間差異有統計學意義(F=28.65 P<0.001).T2DM+AD組GSK-3β錶達水平(4319.02±653.24)顯著高于T2DM組(540.43±558.49)、正常對照組(315.56±91.64)及AD組(304.39±175.83)(H=19.335,P<0.001).AD組(2799.61±1070.02)及T2DM+AD組(8583.814±2236.11)tau蛋白燐痠化錶達水平顯著高于正常對照組(252.024±58.37)及T2DM組(287.75±192.53)(H=32.950,P<0.001). 結論 T2DM大鼠GSK-3β活性的上調可能是引起大鼠tau蛋白燐痠化的一箇重要原因.
목적 연구2형당뇨병(T2DM)병발아이자해묵병(AD)적가능궤제. 방법 선취동령Wistar대서,수궤분위정상대조조、T2DM조、AD조급T2DM+AD조.채용혈당의감측대서혈당,수미궁실험관측대서행위학개변,면역조화염색검측대서당원합성격매-3β(GSK-3β)급tau단백린산화수평. 결과 각모형조대서균교정상대조조학습기억력감퇴,T2DM조여AD조급T2DM+AD조지간차이유통계학의의(F=28.65 P<0.001).T2DM+AD조GSK-3β표체수평(4319.02±653.24)현저고우T2DM조(540.43±558.49)、정상대조조(315.56±91.64)급AD조(304.39±175.83)(H=19.335,P<0.001).AD조(2799.61±1070.02)급T2DM+AD조(8583.814±2236.11)tau단백린산화표체수평현저고우정상대조조(252.024±58.37)급T2DM조(287.75±192.53)(H=32.950,P<0.001). 결론 T2DM대서GSK-3β활성적상조가능시인기대서tau단백린산화적일개중요원인.
Objective To investigate the possible pathogenesis of type 2 diabetes mellitus (T2DM) combined with Alzheimer's disease (AD). Methods Wistar rats were randomly divided into control, T2DM, AD and T2DM +AD groups. The blood glucose levels were assayed, and the behavior changes were tested by Morris water maze. The glycogen synthase kinase-3β (GSK-3β) and hyperphosphorylation of tau protein were detected by immunohistochemistry staining. Results Compared with the control rats, the learning and memory abilities were weakened significantly in the model rats (F=28. 65, P<0.001). The expression of GSK-3β was higher in T2DM + AD group (4319. 02±653. 24) than in AD group (304. 39 ± 175. 83), T2DM group (540.43 ± 558.49) and control group (315. 56 ± 91. 64, H=19. 335, all P<0. 01). The level of hyperphosphorylation of tau protein was significantly increased in T2DM + AD group (8583. 81 ± 2236. 11) and AD group (2799. 61±1070. 02) than in control group (252. 02 ± 58. 37) and T2DM group (287. 75 ± 192. 53, H=32. 950, P< 0.001). There was no significantly difference of hyperphosphorylation of tau between T2DM group and control group (H = 32. 950, P>0. 05). Conclusions The increasing of GSK-3β activity in T2DM may be caused by hyperphosphorylation of tau.
