体育科学
體育科學
체육과학
China Sport Science
2010年
12期
76~81
,共null页
董静梅 陈佩杰 刘举科 余志琪
董靜梅 陳珮傑 劉舉科 餘誌琪
동정매 진패걸 류거과 여지기
大鼠 过度运动 NADPH氧化酶 活性氧 心肌细胞 过氧化损伤 二联苯碘 谷氨酰胺
大鼠 過度運動 NADPH氧化酶 活性氧 心肌細胞 過氧化損傷 二聯苯碘 穀氨酰胺
대서 과도운동 NADPH양화매 활성양 심기세포 과양화손상 이련분전 곡안선알
rat; exhaustive exercise; NADPH oxidase; reactive oxygen species; myocardial cells; oxidative injury; FAS /FASL; DPI; glutamine
目的:探寻过度运动引起的心肌过氧化损伤活性氧产生的途径,实施活性氧产生途径上的干预与营养学上的抗氧化防护,为运动引起的心肌过氧化损伤的抗氧化干预提供方法学上的理论支撑;方法:85只雄性waster大鼠,随机分为安静对照组(C)、单纯过度运动组(E)、过度运动给予DPI干预组(D)、过度运动给予谷氨酰胺干预组(G)、过度运动合并给予DPI与谷氨酰胺干预组(DG),建立过度训练模型后的36h和恢复7天后测定其血浆中的心肌肌钙蛋白(cTnI)、肌酸同工酶(CK-MB)浓度以及心肌组织中的丙二醛(MDA),实时定量PCR测定运动后心肌细胞NADPH氧化酶关键亚基gp91-phox和p22-phox的mRNA的表达;结果:与对照组比较,E组血浆MDA、cTnI、CK-MB均显著升高,恢复7天后显著下降,D、G组则升高幅度低于E组,DG组则变化不明显,但干预组升高的幅度则显著低于单纯训练组。运动后36h的gp91-phox、p22-phox的mRNA的表达也表现出同样的变化特点;结论:过度训练可引起心肌的过氧化损伤,其中,NADPH氧化酶介导产生的活性氧是其过氧损伤的原因之一,NADPH氧化酶的抑制剂与谷氨酰胺合并时使用具有协同的抗氧化防护作用,可有效地防护过度运动引起的心肌过氧化损伤。
目的:探尋過度運動引起的心肌過氧化損傷活性氧產生的途徑,實施活性氧產生途徑上的榦預與營養學上的抗氧化防護,為運動引起的心肌過氧化損傷的抗氧化榦預提供方法學上的理論支撐;方法:85隻雄性waster大鼠,隨機分為安靜對照組(C)、單純過度運動組(E)、過度運動給予DPI榦預組(D)、過度運動給予穀氨酰胺榦預組(G)、過度運動閤併給予DPI與穀氨酰胺榦預組(DG),建立過度訓練模型後的36h和恢複7天後測定其血漿中的心肌肌鈣蛋白(cTnI)、肌痠同工酶(CK-MB)濃度以及心肌組織中的丙二醛(MDA),實時定量PCR測定運動後心肌細胞NADPH氧化酶關鍵亞基gp91-phox和p22-phox的mRNA的錶達;結果:與對照組比較,E組血漿MDA、cTnI、CK-MB均顯著升高,恢複7天後顯著下降,D、G組則升高幅度低于E組,DG組則變化不明顯,但榦預組升高的幅度則顯著低于單純訓練組。運動後36h的gp91-phox、p22-phox的mRNA的錶達也錶現齣同樣的變化特點;結論:過度訓練可引起心肌的過氧化損傷,其中,NADPH氧化酶介導產生的活性氧是其過氧損傷的原因之一,NADPH氧化酶的抑製劑與穀氨酰胺閤併時使用具有協同的抗氧化防護作用,可有效地防護過度運動引起的心肌過氧化損傷。
목적:탐심과도운동인기적심기과양화손상활성양산생적도경,실시활성양산생도경상적간예여영양학상적항양화방호,위운동인기적심기과양화손상적항양화간예제공방법학상적이론지탱;방법:85지웅성waster대서,수궤분위안정대조조(C)、단순과도운동조(E)、과도운동급여DPI간예조(D)、과도운동급여곡안선알간예조(G)、과도운동합병급여DPI여곡안선알간예조(DG),건립과도훈련모형후적36h화회복7천후측정기혈장중적심기기개단백(cTnI)、기산동공매(CK-MB)농도이급심기조직중적병이철(MDA),실시정량PCR측정운동후심기세포NADPH양화매관건아기gp91-phox화p22-phox적mRNA적표체;결과:여대조조비교,E조혈장MDA、cTnI、CK-MB균현저승고,회복7천후현저하강,D、G조칙승고폭도저우E조,DG조칙변화불명현,단간예조승고적폭도칙현저저우단순훈련조。운동후36h적gp91-phox、p22-phox적mRNA적표체야표현출동양적변화특점;결론:과도훈련가인기심기적과양화손상,기중,NADPH양화매개도산생적활성양시기과양손상적원인지일,NADPH양화매적억제제여곡안선알합병시사용구유협동적항양화방호작용,가유효지방호과도운동인기적심기과양화손상。
Objective:To explore the pathways of reactive oxygen species(ROS)induced by exhaustive exercise that damage myocardial cell and to put anti-oxidant intervention into practice with the combination both the way of generating ROS and the nutrition.Methods:85 male Wistar rats were randomly divided into five groups and established protocol of exhaustive exercise.The five groups is sedentary control group(C),exhaustive exercise group(E),exhaustive exercise and DPI intervention group(D),exhaustive exercise and glutamine intervention group(G),exhaustive exercise and the combination of DPI and glutamine intervention group(DG).The concentration ofmalondialdehyde(MDA),cardiac troponin T(cTnT),creatine isoenzyme(CK-MB)in rat blood plasma were determined at 36-40 hours after exhaustive exercise and 7 days recovery respectively.The expression of FAS /FASL of mRNA and the NADPH oxidase subunit gp91-phox p22-phox of mRNA in cardiac myocyte were detected with real-time quantitative PCR.Results:Compared with control group C,the concentration of MDA,cTnI,CK-MB in E group were increased significantly after 7 days recovery were decreased significantly and the concentration in group D and group G also increased no significantly and in DG group did not change.The expression of the FAS /FASL,gp91-phox,p22-Phox of mRNA also showed the same results as the plasma index in all groups at 36h after exercise.Conclusion:The exhaustive training can cause excessive oxidative damage in the heart muscle.The one pathway of ROS generated by NADPH oxidase is the one reasons of the peroxide injury of myocardial cell.So the combination intervention with the inhibitors of NADPH oxidase and glutamine supplement can protect the oxidative injury in myocardial cell induced by exhaustive exercise effectively.