山东体育学院学报
山東體育學院學報
산동체육학원학보
Journal of Shandong Institute Of Physical Education And Sports
2012年
5期
55~61
,共null页
大脑皮质 力竭运动 自由基 超微结构 运动预处理
大腦皮質 力竭運動 自由基 超微結構 運動預處理
대뇌피질 력갈운동 자유기 초미결구 운동예처리
cerebral cortex; exhaustive exercise ; free radicals; ultrastructure; exercise preconditioning
目的:建立SD大鼠运动预处理模型和一次性力竭运动模型,通过观察大鼠大脑皮质微结构、超微结构的变化以及指标测试,探讨运动预处理对一次性力竭后大脑皮质缺血再灌注的保护机制,为科学地进行运动训练提供神经生物学参考依据。方法:选用雄性4月龄SD大鼠70只,适应性喂养1周后随机分为:空白对照组(C组),一次性力竭组(E组)和运动预处理组(EP组),C组、E组大鼠常规喂养6周,EP组采用间歇训练法运动预处理6周。6周后除c组外,其余组大鼠采用一次性力竭训练,并分别在即刻、24小时、48小时取材。测定大鼠脑组织SOD、GSH—PX、MDA;制作切片观察不同时间各组脑组织微结构和超微结构变化。结果:①自由基检测结果:各时相点大鼠脑组织EP组SOD,GSH—PX活性均显著性高于C组和E组(P〈0.05);其中EP组在即刻较其它组出现非常显著性(P〈0.01),而在第2个时相点E组和EP组均出现非常显著性下降(P〈0.01),在第3个时相点出现显著性上升(P〈0.05);E组和EP组之间MDA含量没有显著性差(P〉0.05),但是E组MDA含量却高于EP组②大鼠大脑皮质微结构和超微结构结果:EP组各时相点神经元细胞核损伤、线粒体损伤均明显好于E组。结论:运动预处理可提高力竭运动后大脑组织SOD、GSH—PX活性,减轻脂质过氧化程度,提高大脑清除自由基能力,从而有效预防一次性力竭运动造成的脑缺血再灌注损伤,起到对机体的内源性保护作用。
目的:建立SD大鼠運動預處理模型和一次性力竭運動模型,通過觀察大鼠大腦皮質微結構、超微結構的變化以及指標測試,探討運動預處理對一次性力竭後大腦皮質缺血再灌註的保護機製,為科學地進行運動訓練提供神經生物學參攷依據。方法:選用雄性4月齡SD大鼠70隻,適應性餵養1週後隨機分為:空白對照組(C組),一次性力竭組(E組)和運動預處理組(EP組),C組、E組大鼠常規餵養6週,EP組採用間歇訓練法運動預處理6週。6週後除c組外,其餘組大鼠採用一次性力竭訓練,併分彆在即刻、24小時、48小時取材。測定大鼠腦組織SOD、GSH—PX、MDA;製作切片觀察不同時間各組腦組織微結構和超微結構變化。結果:①自由基檢測結果:各時相點大鼠腦組織EP組SOD,GSH—PX活性均顯著性高于C組和E組(P〈0.05);其中EP組在即刻較其它組齣現非常顯著性(P〈0.01),而在第2箇時相點E組和EP組均齣現非常顯著性下降(P〈0.01),在第3箇時相點齣現顯著性上升(P〈0.05);E組和EP組之間MDA含量沒有顯著性差(P〉0.05),但是E組MDA含量卻高于EP組②大鼠大腦皮質微結構和超微結構結果:EP組各時相點神經元細胞覈損傷、線粒體損傷均明顯好于E組。結論:運動預處理可提高力竭運動後大腦組織SOD、GSH—PX活性,減輕脂質過氧化程度,提高大腦清除自由基能力,從而有效預防一次性力竭運動造成的腦缺血再灌註損傷,起到對機體的內源性保護作用。
목적:건립SD대서운동예처리모형화일차성력갈운동모형,통과관찰대서대뇌피질미결구、초미결구적변화이급지표측시,탐토운동예처리대일차성력갈후대뇌피질결혈재관주적보호궤제,위과학지진행운동훈련제공신경생물학삼고의거。방법:선용웅성4월령SD대서70지,괄응성위양1주후수궤분위:공백대조조(C조),일차성력갈조(E조)화운동예처리조(EP조),C조、E조대서상규위양6주,EP조채용간헐훈련법운동예처리6주。6주후제c조외,기여조대서채용일차성력갈훈련,병분별재즉각、24소시、48소시취재。측정대서뇌조직SOD、GSH—PX、MDA;제작절편관찰불동시간각조뇌조직미결구화초미결구변화。결과:①자유기검측결과:각시상점대서뇌조직EP조SOD,GSH—PX활성균현저성고우C조화E조(P〈0.05);기중EP조재즉각교기타조출현비상현저성(P〈0.01),이재제2개시상점E조화EP조균출현비상현저성하강(P〈0.01),재제3개시상점출현현저성상승(P〈0.05);E조화EP조지간MDA함량몰유현저성차(P〉0.05),단시E조MDA함량각고우EP조②대서대뇌피질미결구화초미결구결과:EP조각시상점신경원세포핵손상、선립체손상균명현호우E조。결론:운동예처리가제고력갈운동후대뇌조직SOD、GSH—PX활성,감경지질과양화정도,제고대뇌청제자유기능력,종이유효예방일차성력갈운동조성적뇌결혈재관주손상,기도대궤체적내원성보호작용。
Objective : In this study the establishment of SD rat model and a one - time pre - movement model of exhaustive exercise, by observing the micro - structure of rat cerebral cortex, ultrastructur- al changes, and indicators of exercise tests on a one - time pre - exhausted cerebral cortex caused by lack of blood- reperfusion injury protection mechanisms, in order to provide a scientific reference for exercise training. After adaptive feeding for 1 week,70 four - month - old SD male rats were randomly divided into three major groups : the control group ( C group), a one - time exhaustive group (E group), exercise preconditioning group (EP group). C group and E group were fed 6 weeks routinely, while EP group were pretreated 6 weeks by intermittent training. 6 weeks later, all groups except C group took an exhaustive swimming training, and separately selected sampling in- stantly, 24 hours, 48 hours after training. SOD, GSH - PX activity and MDA levels of rats cerebral cortex were detected, and rat cerebral cortex micro -structure and ultrastructure observed in defer- ent time by sections. Results: (2)Compared with C and E group, SOD and GSH -PX activity of EP group were obviously higher at deferent time points, especially very significantly higher than the oth- er groups (P 〈0.01)at instant time. While SOD and GSH- PX activity of E and EP group de- creased significantly at the second time point (P 〈0.01 ) and obviously increased again at the third time point (P 〈 0.05). Compared with EP group, MDA content of E group was no obviously differ- ent, while MDA content of E group was higher. (2)Rat cerebral cortex micro - structure and ultra- structure : The injuring of neuron nucleus and mitochondrion those in EP group were all smaller than in E group at each time point, which indicated that high -intensity interval training can be effective in preventing a result of a one - time exhausted the body's ability to get rid of free radicals. cerebral ischemia- reperfusion injury and enhance