解放军医药杂志
解放軍醫藥雜誌
해방군의약잡지
MEDICAL&PHARMACEUTICAL JOURNAL OF CHINESE PEOPLE'S LIBERATION ARMY
2015年
2期
42-46
,共5页
胡丽叶%陈红军%宋光耀%朱旅云
鬍麗葉%陳紅軍%宋光耀%硃旅雲
호려협%진홍군%송광요%주려운
糖尿病,2型%内皮型一氧化氮合酶%主动脉%罗格列酮%大鼠, Wistar
糖尿病,2型%內皮型一氧化氮閤酶%主動脈%囉格列酮%大鼠, Wistar
당뇨병,2형%내피형일양화담합매%주동맥%라격렬동%대서, Wistar
Diabetes mellitus,type 2%Endothelia nitric oxide synthase%Aorta%Rosiglitazone%Rats,Wistar
目的：观察2型糖尿病(T2DM)大鼠血清内皮素、一氧化氮水平，主动脉病理变化、内皮型一氧化氮合酶( eNOS)蛋白及其mRNA的表达，探讨噻唑烷二酮类药物的干预作用。方法雄性Wistar大鼠80只，随机分为对照组、高脂组、模型组、治疗组各20只，制备T2DM大鼠模型后，治疗组予罗格列酮灌胃治疗，分别于给药6和12周时取样进行血糖、血脂、内皮素、一氧化氮的检测，观察光镜下主动脉的病理变化，主动脉eNOS蛋白及其mRNA表达情况。结果给药6、12周高脂组、模型组及治疗组较对照组内皮素升高，一氧化氮降低( P<0．01)。给药12周时模型组较高脂组和治疗组内皮素升高，一氧化氮降低( P<0．05)。给药12周时模型组一氧化氮水平较给药6周时下降( P<0．05)。给药12周时高脂组、模型组和治疗组大鼠主动脉出现不同程度病理改变。给药6和12周时，主动脉eNOS的蛋白和mRNA表达高脂组、模型组和治疗组较对照组下调，且12周时模型组较高脂组下调( P<0．01)。结论高血糖、高血脂可导致内皮素升高和一氧化氮下降，以及eNOS蛋白及其mRNA表达异常，从而引起动脉硬化，噻唑烷二酮类药物对血管内皮功能、病理形态、eNOS蛋白及其mRNA表达异常有一定逆转作用。
目的：觀察2型糖尿病(T2DM)大鼠血清內皮素、一氧化氮水平，主動脈病理變化、內皮型一氧化氮閤酶( eNOS)蛋白及其mRNA的錶達，探討噻唑烷二酮類藥物的榦預作用。方法雄性Wistar大鼠80隻，隨機分為對照組、高脂組、模型組、治療組各20隻，製備T2DM大鼠模型後，治療組予囉格列酮灌胃治療，分彆于給藥6和12週時取樣進行血糖、血脂、內皮素、一氧化氮的檢測，觀察光鏡下主動脈的病理變化，主動脈eNOS蛋白及其mRNA錶達情況。結果給藥6、12週高脂組、模型組及治療組較對照組內皮素升高，一氧化氮降低( P<0．01)。給藥12週時模型組較高脂組和治療組內皮素升高，一氧化氮降低( P<0．05)。給藥12週時模型組一氧化氮水平較給藥6週時下降( P<0．05)。給藥12週時高脂組、模型組和治療組大鼠主動脈齣現不同程度病理改變。給藥6和12週時，主動脈eNOS的蛋白和mRNA錶達高脂組、模型組和治療組較對照組下調，且12週時模型組較高脂組下調( P<0．01)。結論高血糖、高血脂可導緻內皮素升高和一氧化氮下降，以及eNOS蛋白及其mRNA錶達異常，從而引起動脈硬化，噻唑烷二酮類藥物對血管內皮功能、病理形態、eNOS蛋白及其mRNA錶達異常有一定逆轉作用。
목적：관찰2형당뇨병(T2DM)대서혈청내피소、일양화담수평，주동맥병리변화、내피형일양화담합매( eNOS)단백급기mRNA적표체，탐토새서완이동류약물적간예작용。방법웅성Wistar대서80지，수궤분위대조조、고지조、모형조、치료조각20지，제비T2DM대서모형후，치료조여라격렬동관위치료，분별우급약6화12주시취양진행혈당、혈지、내피소、일양화담적검측，관찰광경하주동맥적병리변화，주동맥eNOS단백급기mRNA표체정황。결과급약6、12주고지조、모형조급치료조교대조조내피소승고，일양화담강저( P<0．01)。급약12주시모형조교고지조화치료조내피소승고，일양화담강저( P<0．05)。급약12주시모형조일양화담수평교급약6주시하강( P<0．05)。급약12주시고지조、모형조화치료조대서주동맥출현불동정도병리개변。급약6화12주시，주동맥eNOS적단백화mRNA표체고지조、모형조화치료조교대조조하조，차12주시모형조교고지조하조( P<0．01)。결론고혈당、고혈지가도치내피소승고화일양화담하강，이급eNOS단백급기mRNA표체이상，종이인기동맥경화，새서완이동류약물대혈관내피공능、병리형태、eNOS단백급기mRNA표체이상유일정역전작용。
Objective To observe of serum endothelin ( ET) , nitric oxide level, aortic pathological changes and expressions of aortic endothelial nitric oxide (NO) synthase (eNOS) and mRNA (messenger ribonucleic acid) in rats with type 2 diabetes mellitus (T2DM), and to investigate the intervention effect of thiazolidinediones. Methods A total of 80 male Wistar rats were randomly divided into control group, high fat diet group, model group and treatment group ( n=20 for each group) . After the type 2 diabetes mellitus models were successfully established, the treatment group was lavaged with Rosiglitazone. In 6th and 12th weeks of administration, levels of blood glucose, blood lipid, endothelin and nitric oxide were tested in blood samples, and aortic pathological changes were observed under the light microscope. Meanwhile, the expressions of aortic eNOS protein and mRNA were also studied in the four groups. Results Compared with those in control group, in 6th and 12th weeks of administration, ET levels were increased, and the NO levels were de-creased significantly in high fat diet, model group and treatment groups. In the 12th week of administration, ET level was increased, while NO level was significantly decreased in model group than those in high fat diet and treatment groups ( P<0. 05). Compared with that in the 6th week of administration, the NO level in the 12th week of administration was signifi-cantly decreased in model group (P<0. 05). In the 12th week of administration, different degrees of pathological changes were observed in high fat diet, model and treatment groups. Compared with those in control group, expressions of protein eNOS and mRNA in high fat diet, model and treatment groups were decreased in 6th and 12th weeks of administration, and changes in model group in the 12th week of administration were more significant than those in high fat diet group ( P<0. 01). Conclusion Hyperglycemia and hyperlipemia may induce the increase of ET level, decreased NO level and abnor-mal expressions of protein eNOS and mRNA, which may cause atherosclerosis. Thiazolidinediones have a certain reverse effect on vascular endothelium function, pathological morphous and abnormal expressions of protein eNOS and mRNA.
