中华临床医师杂志(电子版)
中華臨床醫師雜誌(電子版)
중화림상의사잡지(전자판)
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
4期
1661-1664
,共4页
曹建雷%熊世熙%龚斐%王海蓉%干学东%吴晓燕%卫银芝%汪瀚
曹建雷%熊世熙%龔斐%王海蓉%榦學東%吳曉燕%衛銀芝%汪瀚
조건뢰%웅세희%공비%왕해용%간학동%오효연%위은지%왕한
糖尿病%大鼠%心室功能,左%血管紧张素Ⅱ%Fas配体蛋白质%贝那普利
糖尿病%大鼠%心室功能,左%血管緊張素Ⅱ%Fas配體蛋白質%貝那普利
당뇨병%대서%심실공능,좌%혈관긴장소Ⅱ%Fas배체단백질%패나보리
Diabetes mellitus%Rats%Ventricular function,left%AngiotensinⅡ%Fas ligand protein%Benazepril
目的通过观察糖尿病大鼠心功能的变化,探讨贝那普利对其可能的影响机制。方法30只SD大鼠随机分为空白对照组(n=10)和糖尿病模型组(n=20),糖尿病组用链脲佐菌素(STZ)腹腔注射建模,成功后再随机分为糖尿病对照组(n=10)和贝那普利治疗组(n=10)。治疗组给予贝那普利10 mg· kg-1· d-1灌胃,糖尿病对照组和空白对照组给予相同体积的生理盐水灌胃。给药9周后,彩色多普勒超声检测心功能,SP免疫组化法检测心肌组织Fas蛋白表达率,放射免疫法检测心肌局部血管紧张素Ⅱ( AngⅡ)含量,电镜下观察心肌超微结构变化。结果与空白对照组相比,糖尿病模型组AngⅡ的含量明显增多(4340.67±348.37 vs.5367.43±498.28,P<0.01),Fas蛋白表达率明显升高[(1.87±0.73)% vs.(35.68±0.79)%,P<0.01];与糖尿病模型组对比,贝那普利治疗组可显著降低AngⅡ含量,降低Fas 蛋白表达[5367.43±498.28 vs.4501.50±129.33,P<0.01;(35.68±0.79)%vs.(28.00±0.63)%,P<0.05];应用贝那普利治疗后,可有效改善心功能( P<0.01)。结论糖尿病大鼠心功能明显降低,贝那普利则可通过降低AngⅡ、Fas蛋白表达改善心功能。
目的通過觀察糖尿病大鼠心功能的變化,探討貝那普利對其可能的影響機製。方法30隻SD大鼠隨機分為空白對照組(n=10)和糖尿病模型組(n=20),糖尿病組用鏈脲佐菌素(STZ)腹腔註射建模,成功後再隨機分為糖尿病對照組(n=10)和貝那普利治療組(n=10)。治療組給予貝那普利10 mg· kg-1· d-1灌胃,糖尿病對照組和空白對照組給予相同體積的生理鹽水灌胃。給藥9週後,綵色多普勒超聲檢測心功能,SP免疫組化法檢測心肌組織Fas蛋白錶達率,放射免疫法檢測心肌跼部血管緊張素Ⅱ( AngⅡ)含量,電鏡下觀察心肌超微結構變化。結果與空白對照組相比,糖尿病模型組AngⅡ的含量明顯增多(4340.67±348.37 vs.5367.43±498.28,P<0.01),Fas蛋白錶達率明顯升高[(1.87±0.73)% vs.(35.68±0.79)%,P<0.01];與糖尿病模型組對比,貝那普利治療組可顯著降低AngⅡ含量,降低Fas 蛋白錶達[5367.43±498.28 vs.4501.50±129.33,P<0.01;(35.68±0.79)%vs.(28.00±0.63)%,P<0.05];應用貝那普利治療後,可有效改善心功能( P<0.01)。結論糖尿病大鼠心功能明顯降低,貝那普利則可通過降低AngⅡ、Fas蛋白錶達改善心功能。
목적통과관찰당뇨병대서심공능적변화,탐토패나보리대기가능적영향궤제。방법30지SD대서수궤분위공백대조조(n=10)화당뇨병모형조(n=20),당뇨병조용련뇨좌균소(STZ)복강주사건모,성공후재수궤분위당뇨병대조조(n=10)화패나보리치료조(n=10)。치료조급여패나보리10 mg· kg-1· d-1관위,당뇨병대조조화공백대조조급여상동체적적생리염수관위。급약9주후,채색다보륵초성검측심공능,SP면역조화법검측심기조직Fas단백표체솔,방사면역법검측심기국부혈관긴장소Ⅱ( AngⅡ)함량,전경하관찰심기초미결구변화。결과여공백대조조상비,당뇨병모형조AngⅡ적함량명현증다(4340.67±348.37 vs.5367.43±498.28,P<0.01),Fas단백표체솔명현승고[(1.87±0.73)% vs.(35.68±0.79)%,P<0.01];여당뇨병모형조대비,패나보리치료조가현저강저AngⅡ함량,강저Fas 단백표체[5367.43±498.28 vs.4501.50±129.33,P<0.01;(35.68±0.79)%vs.(28.00±0.63)%,P<0.05];응용패나보리치료후,가유효개선심공능( P<0.01)。결론당뇨병대서심공능명현강저,패나보리칙가통과강저AngⅡ、Fas단백표체개선심공능。
Objective To explore the possible mechanism about benazepril improving the heart function of diabetic rats.Methods 30 SD rats were randomly divided into 2 groups,10 as normal control group and the other 20 as diabetic group which were induced by STZ ,after the models were constructed successfully ,randomly devided into diabetic control group, benazepril treated group, each contains 10.Following the instruction, benazepril was administrated at the concentration of 10 mg/kg once a day ,while in the diabetic control group and the normal control the same volume sodium chloride was administrated .Nine weeks later , heart function was detected by Doppler echocardiography ,SP immunohistochemical staining was used to detect the level of Fas , radioimmunity was used to measure the content of AngⅡ, transmission electron microscope was used to observe the changes of cardiocyte . Results Compared to the normal control group ,the content of AngⅡincreased significantly (4340.67 ±348.37 vs. 5367.43 ±498.28,P<0.01),the rate of expression of Fas increased significantly [(1.87 ±0.73)%vs.(35.68 ± 0.79)%,P <0.01],benazepril could decrease the above (P <0.05).Compared to the diabetic control group, benazepril treated group could decreased the expression of AngⅡand Fas[5367.43 ±498.28 vs.4501.50 ±129.33 , P<0.01;( 35.68 ±0.79 )% vs.( 28.00 ±0.63 )%, P <0.05 ] , and it also could improve the heart function . Conclusions The heart function in benazepril treated group decreased significantly , it could improve the heart function through decreasing the content of AngⅡand Fas.