体育学刊
體育學刊
체육학간
Journal of Physical Education
2013年
2期
130~134
,共null页
运动生物化学 2型糖尿病 运动训练 心肌纤维化 氧化应激 大鼠
運動生物化學 2型糖尿病 運動訓練 心肌纖維化 氧化應激 大鼠
운동생물화학 2형당뇨병 운동훈련 심기섬유화 양화응격 대서
sports biochemistry; type 2 diabetes; exercising; myocardial fibrosis; oxidative stress; rats
通过高脂喂养加腹腔注射小剂量链脲佐菌素（STZ）构建2型糖尿病大鼠模型,探讨运动训练对2型糖尿病大鼠心肌纤维化的改善作用。结果发现：与正常对照组相比,糖尿病对照组血液GLU、GHb、GSP和INS水平及心肌AGEs、Hyp、CVF、GSSG/GSH、MDA和NF-κB P65蛋白表达均显著升高（P〈0.05或P〈0.01）;与糖尿病对照组相比,糖尿病运动组（DE）的血液GLU、GHb和GSP水平及心肌AGEs、Hyp、CVF、GSSG/GSH、MDA和NF-κB P65蛋白表达均显著降低（P〈0.05或P〈0.01）。结果表明：本实验所复制的2型糖尿病大鼠模型存在心肌纤维化的现象,运动可改善2型糖尿病大鼠空腹血糖,降低心肌组织AGEs含量、氧化应激和NF-κB P65蛋白表达水平,对糖尿病大鼠心肌纤维化起到改善作用,AGEs/氧化应激/NF-κB P65可能为运动改善2型糖尿病大鼠心肌纤维化的重要通路。
通過高脂餵養加腹腔註射小劑量鏈脲佐菌素（STZ）構建2型糖尿病大鼠模型,探討運動訓練對2型糖尿病大鼠心肌纖維化的改善作用。結果髮現：與正常對照組相比,糖尿病對照組血液GLU、GHb、GSP和INS水平及心肌AGEs、Hyp、CVF、GSSG/GSH、MDA和NF-κB P65蛋白錶達均顯著升高（P〈0.05或P〈0.01）;與糖尿病對照組相比,糖尿病運動組（DE）的血液GLU、GHb和GSP水平及心肌AGEs、Hyp、CVF、GSSG/GSH、MDA和NF-κB P65蛋白錶達均顯著降低（P〈0.05或P〈0.01）。結果錶明：本實驗所複製的2型糖尿病大鼠模型存在心肌纖維化的現象,運動可改善2型糖尿病大鼠空腹血糖,降低心肌組織AGEs含量、氧化應激和NF-κB P65蛋白錶達水平,對糖尿病大鼠心肌纖維化起到改善作用,AGEs/氧化應激/NF-κB P65可能為運動改善2型糖尿病大鼠心肌纖維化的重要通路。
통과고지위양가복강주사소제량련뇨좌균소（STZ）구건2형당뇨병대서모형,탐토운동훈련대2형당뇨병대서심기섬유화적개선작용。결과발현：여정상대조조상비,당뇨병대조조혈액GLU、GHb、GSP화INS수평급심기AGEs、Hyp、CVF、GSSG/GSH、MDA화NF-κB P65단백표체균현저승고（P〈0.05혹P〈0.01）;여당뇨병대조조상비,당뇨병운동조（DE）적혈액GLU、GHb화GSP수평급심기AGEs、Hyp、CVF、GSSG/GSH、MDA화NF-κB P65단백표체균현저강저（P〈0.05혹P〈0.01）。결과표명：본실험소복제적2형당뇨병대서모형존재심기섬유화적현상,운동가개선2형당뇨병대서공복혈당,강저심기조직AGEs함량、양화응격화NF-κB P65단백표체수평,대당뇨병대서심기섬유화기도개선작용,AGEs/양화응격/NF-κB P65가능위운동개선2형당뇨병대서심기섬유화적중요통로。
The authors established a type 2 diabetic rat model by means of high fat feeding plus intraperitoneal injection of a small dose of streptozotocin（STZ）,probed into the role of exercising in improving the myocardial fibrosis of type 2 diabetic rats,and revealed the following findings： as compared with those of the rats in the normal control group,the blood GLU,GHb,GSP and INS level as well as myocardium AGEs,Hyp,CVF,GSSG/GSH,MDA and NF-κB P65 protein expression of the rats in the diabetic control group increased significantly（P0.05 or P0.01）;as compared with those of the rats in the diabetic control group,the blood GLU,GHb and GSP level as well as myocardium AGEs,Hyp,CVF,GSSG/GSH,MDA and NF-κB P65 protein expression of the rats in the diabetic exercising group decreased significantly（P0.05 or P0.01）.The said findings indicated the followings： the type 2 diabetic rat model duplicated by this experiment showed such a sign as myocardial fibrosis;exercising could improve the fasting blood glucose of type 2 diabetic rats,lower myocardial tissue’s AGEs content,oxidative stress and the level of NF-κB P65 protein expression,play a role in improving the myocardial fibrosis of type 2 diabetic rats;AGEs or oxidative stress or NF-κB P65 might be an important channel for exercising to improve the myocardial fibrosis of type 2 diabetic rats.
