交通医学
交通醫學
교통의학
MEDICAL JOURNAL OF COMMUNICATIONS
2014年
6期
586-589
,共4页
糖尿病%阿尔茨海默病%Morris水迷宫%tau蛋白%链脲佐菌素%蛋白免疫印迹法%叶酸%维生素B12
糖尿病%阿爾茨海默病%Morris水迷宮%tau蛋白%鏈脲佐菌素%蛋白免疫印跡法%葉痠%維生素B12
당뇨병%아이자해묵병%Morris수미궁%tau단백%련뇨좌균소%단백면역인적법%협산%유생소B12
Alzheimer’s disease%diabetes mellitus%Morris water maze%tau%folic acid%vitamin B12
目的：研究糖尿病大鼠脑内各磷酸化位点的变化，探讨叶酸联合维生素B12对糖尿病模型大鼠学习记忆能力及脑内tau蛋白过度磷酸化的影响。方法：糖尿病大鼠用链脲佐菌素腹腔注射制备，实验组予以叶酸联合维生素B12干预。采用Morris水迷宫检测各组大鼠空间记忆及学习能力；用蛋白免疫印迹法观察各组大鼠额叶皮层脑组织总tau、tau部分位点磷酸化变化。结果：（1）Morris水迷宫结果：1型、2型糖尿病组大鼠逃避潜伏期较对照组及单纯药物干预组明显延长（P<0.05），使用叶酸联合维生素B12干预相应模型组后均能显著改善（P<0.05）。（2）叶酸联合维生素B12对糖尿病大鼠脑内tau蛋白过度磷酸化影响：各组大鼠额叶皮层脑组织总tau蛋白含量比较差异无统计学意义（P>0.05）；1型、2型糖尿病组大鼠额叶皮层脑组织tau蛋白在丝氨酸396/404位点、苏氨酸205位点、苏氨酸212位点的磷酸化水平较对照组及单纯药物干预组明显增高，差异有统计学意义（P<0.05），使用叶酸联合维生素B12干预后，以上位点磷酸化水平均有明显下降（P<0.05）。结论：糖尿病大鼠脑组织内tau蛋白出现阿尔茨海默病样过度磷酸化；叶酸联合维生素B12干预后可逆转病变，发挥保护脑组织作用。
目的：研究糖尿病大鼠腦內各燐痠化位點的變化，探討葉痠聯閤維生素B12對糖尿病模型大鼠學習記憶能力及腦內tau蛋白過度燐痠化的影響。方法：糖尿病大鼠用鏈脲佐菌素腹腔註射製備，實驗組予以葉痠聯閤維生素B12榦預。採用Morris水迷宮檢測各組大鼠空間記憶及學習能力；用蛋白免疫印跡法觀察各組大鼠額葉皮層腦組織總tau、tau部分位點燐痠化變化。結果：（1）Morris水迷宮結果：1型、2型糖尿病組大鼠逃避潛伏期較對照組及單純藥物榦預組明顯延長（P<0.05），使用葉痠聯閤維生素B12榦預相應模型組後均能顯著改善（P<0.05）。（2）葉痠聯閤維生素B12對糖尿病大鼠腦內tau蛋白過度燐痠化影響：各組大鼠額葉皮層腦組織總tau蛋白含量比較差異無統計學意義（P>0.05）；1型、2型糖尿病組大鼠額葉皮層腦組織tau蛋白在絲氨痠396/404位點、囌氨痠205位點、囌氨痠212位點的燐痠化水平較對照組及單純藥物榦預組明顯增高，差異有統計學意義（P<0.05），使用葉痠聯閤維生素B12榦預後，以上位點燐痠化水平均有明顯下降（P<0.05）。結論：糖尿病大鼠腦組織內tau蛋白齣現阿爾茨海默病樣過度燐痠化；葉痠聯閤維生素B12榦預後可逆轉病變，髮揮保護腦組織作用。
목적：연구당뇨병대서뇌내각린산화위점적변화，탐토협산연합유생소B12대당뇨병모형대서학습기억능력급뇌내tau단백과도린산화적영향。방법：당뇨병대서용련뇨좌균소복강주사제비，실험조여이협산연합유생소B12간예。채용Morris수미궁검측각조대서공간기억급학습능력；용단백면역인적법관찰각조대서액협피층뇌조직총tau、tau부분위점린산화변화。결과：（1）Morris수미궁결과：1형、2형당뇨병조대서도피잠복기교대조조급단순약물간예조명현연장（P<0.05），사용협산연합유생소B12간예상응모형조후균능현저개선（P<0.05）。（2）협산연합유생소B12대당뇨병대서뇌내tau단백과도린산화영향：각조대서액협피층뇌조직총tau단백함량비교차이무통계학의의（P>0.05）；1형、2형당뇨병조대서액협피층뇌조직tau단백재사안산396/404위점、소안산205위점、소안산212위점적린산화수평교대조조급단순약물간예조명현증고，차이유통계학의의（P<0.05），사용협산연합유생소B12간예후，이상위점린산화수평균유명현하강（P<0.05）。결론：당뇨병대서뇌조직내tau단백출현아이자해묵병양과도린산화；협산연합유생소B12간예후가역전병변，발휘보호뇌조직작용。
Object ive:To investigate the changes of hyperphosphorylation of tau in the brain of diabetes mellitus model rats and to determine whether the supplementation of folic acid and vitamin B12 prevents the AD-like hyperphospho_rylation of tau in the diabetes rat brain and leaning and memory deficits, which may provide a theory reference for the clin_ical application. Methods:Diabetes mellitus rats were induced by intraperitoneal injection Streptozocin, and the treatment groups were treated with folic acid/vitamineB12. The spatial memory and learning ability was tested by the Morris water maze. Western blot was used to detect the level of some proteins such as total tau and phosphorylation of tau at some sites. Results:(1)Results of Morris water maze:both type I diabetes mellitus(T1DM) and type II diabetes mellitus(T2DM) rats had much longer escape latency (P<0.05), and the time of escape latency was significantly shortened in the diabetes rats which received the supplementation of folic acid and vitamin B12(P<0.05).(2)Effect of supplementation of folic acid and vitamin B12 on the abnormal hyperphosphorylation of tau in diabetes mellitus rats: the level of tau in the frontal cortex of brain had no difference (P>0.05);the levels of phosphorylated tau at serine 396/404, threonine 205 and threonine 212 were increased in both T1DM group and T2DM group(P<0.05), suggesting the hypeprhosphorylation of tau in diabetes rat brain. Supplementa_tion of folic acid and vitamin B12 attenuated hyperphosphorylation significantly at the above sites (P<0.05). Conclusion: It was showed in the test that the spatial memory and learning ability of T1DM group and T2DM rats was impaired signifi_cantly, and Tau in the brain of DM model rats was hyperphosphorylated. Both of them were improved by supplementation of folic acid and vitamin B12.
