CAJ | 학술논문

背景:不少医学研究表明,细胞凋亡能导致大量自由基增多、Ca~(2+)浓度升高、线粒体膜电位下降引起运动能力的下降.因此,研究细胞凋亡与运动训练的关系意义重要.目的:总结与探索关于肌肉运动与骨骼肌细胞凋亡的相关问题.方法:计算机检索中国期刊全文数据(网址http://dlib.cnki.net/kns50/index.aspx)及PubMed数据库(网址http://www.ncbi.nlm.nih.gov/pubmed/)1990-01/2009-06期间的相关文章,检索词为"肌肉运动,骨骼肌细胞凋亡,muscle exercise,apoptosis in the skeletal muscle".纳入与肌肉运动与骨骼肌细胞的凋亡研究现状与发展密切相关.①有关骨骼肌细胞凋亡的研究.②运动与骨骼肌细胞凋亡研究.③运动诱发骨骼肌细胞凋亡的基因调控研究.④骨骼肌细胞凋亡的分子机制研究.⑤同一领域选择近期发表或在权威杂志上发表的文章.排除重复性研究.结果与结论:运动后,正常肌肉中或是病理状态下的肌肉中骨骼肌细胞都会出现凋亡,凋亡的形态学表现与普通凋亡细胞相似,即核固缩、质膜发泡、细胞器紧缩,凋亡小体形成,其凋亡过程大致可分为3个阶段,即启始阶段、效应阶段和降解阶段.骨骼肌细胞凋亡的增加是导致运动性疲劳的重要原因.目前国内外对骨骼肌细胞凋亡的基因调控研究主要是从凋亡调控因子Bcl-2蛋白、肿瘤坏死因子α及死亡蛋白酶半胱氨酸天冬氨酸酶着手.bcl-2基因蛋白的抗凋亡作用主要是通过阻止线粒体通透性转换孔的开放,阻止线粒体释放促凋亡蛋白、防止线粒体膜脂质过氧化以及线粒体基质Ca2+释放实现的.肿瘤坏死因子家族在启动死亡因子及其受体途径中起重要作用,此途径的启动依赖于死亡配体与死亡受体相结合,激活半胱氨酸天冬氨酸酶,导致细胞凋亡.通过研究探索运动强度与骨骼肌细胞凋亡及坏死的界限关系,有利于在运动中认识运动性疲劳产生的机制及有效消除疲劳. 揹景:不少醫學研究錶明,細胞凋亡能導緻大量自由基增多、Ca~(2+)濃度升高、線粒體膜電位下降引起運動能力的下降.因此,研究細胞凋亡與運動訓練的關繫意義重要.目的:總結與探索關于肌肉運動與骨骼肌細胞凋亡的相關問題.方法:計算機檢索中國期刊全文數據(網阯http://dlib.cnki.net/kns50/index.aspx)及PubMed數據庫(網阯http://www.ncbi.nlm.nih.gov/pubmed/)1990-01/2009-06期間的相關文章,檢索詞為"肌肉運動,骨骼肌細胞凋亡,muscle exercise,apoptosis in the skeletal muscle".納入與肌肉運動與骨骼肌細胞的凋亡研究現狀與髮展密切相關.①有關骨骼肌細胞凋亡的研究.②運動與骨骼肌細胞凋亡研究.③運動誘髮骨骼肌細胞凋亡的基因調控研究.④骨骼肌細胞凋亡的分子機製研究.⑤同一領域選擇近期髮錶或在權威雜誌上髮錶的文章.排除重複性研究.結果與結論:運動後,正常肌肉中或是病理狀態下的肌肉中骨骼肌細胞都會齣現凋亡,凋亡的形態學錶現與普通凋亡細胞相似,即覈固縮、質膜髮泡、細胞器緊縮,凋亡小體形成,其凋亡過程大緻可分為3箇階段,即啟始階段、效應階段和降解階段.骨骼肌細胞凋亡的增加是導緻運動性疲勞的重要原因.目前國內外對骨骼肌細胞凋亡的基因調控研究主要是從凋亡調控因子Bcl-2蛋白、腫瘤壞死因子α及死亡蛋白酶半胱氨痠天鼕氨痠酶著手.bcl-2基因蛋白的抗凋亡作用主要是通過阻止線粒體通透性轉換孔的開放,阻止線粒體釋放促凋亡蛋白、防止線粒體膜脂質過氧化以及線粒體基質Ca2+釋放實現的.腫瘤壞死因子傢族在啟動死亡因子及其受體途徑中起重要作用,此途徑的啟動依賴于死亡配體與死亡受體相結閤,激活半胱氨痠天鼕氨痠酶,導緻細胞凋亡.通過研究探索運動彊度與骨骼肌細胞凋亡及壞死的界限關繫,有利于在運動中認識運動性疲勞產生的機製及有效消除疲勞.
배경:불소의학연구표명,세포조망능도치대량자유기증다、Ca~(2+)농도승고、선립체막전위하강인기운동능력적하강.인차,연구세포조망여운동훈련적관계의의중요.목적:총결여탐색관우기육운동여골격기세포조망적상관문제.방법:계산궤검색중국기간전문수거(망지http://dlib.cnki.net/kns50/index.aspx)급PubMed수거고(망지http://www.ncbi.nlm.nih.gov/pubmed/)1990-01/2009-06기간적상관문장,검색사위"기육운동,골격기세포조망,muscle exercise,apoptosis in the skeletal muscle".납입여기육운동여골격기세포적조망연구현상여발전밀절상관.①유관골격기세포조망적연구.②운동여골격기세포조망연구.③운동유발골격기세포조망적기인조공연구.④골격기세포조망적분자궤제연구.⑤동일영역선택근기발표혹재권위잡지상발표적문장.배제중복성연구.결과여결론:운동후,정상기육중혹시병리상태하적기육중골격기세포도회출현조망,조망적형태학표현여보통조망세포상사,즉핵고축、질막발포、세포기긴축,조망소체형성,기조망과정대치가분위3개계단,즉계시계단、효응계단화강해계단.골격기세포조망적증가시도치운동성피로적중요원인.목전국내외대골격기세포조망적기인조공연구주요시종조망조공인자Bcl-2단백、종류배사인자α급사망단백매반광안산천동안산매착수.bcl-2기인단백적항조망작용주요시통과조지선립체통투성전환공적개방,조지선립체석방촉조망단백、방지선립체막지질과양화이급선립체기질Ca2+석방실현적.종류배사인자가족재계동사망인자급기수체도경중기중요작용,차도경적계동의뢰우사망배체여사망수체상결합,격활반광안산천동안산매,도치세포조망.통과연구탐색운동강도여골격기세포조망급배사적계한관계,유리우재운동중인식운동성피로산생적궤제급유효소제피로.
BACKGROUND:Studies have shown that cell apoptosis can increase free radical,elevate Ca~(2+) concentration,and decrease mitochondrial membrane potential,ultimately reducing motor function.Therefore,understanding of relationship between apoptosis and exercise training is very important. OBJECTIVE:To summarize questions recording muscle exercise and apoptosis in skeletal muscle.METHODS:A computer-based online search of CNKI (http://dlib.cnki.net/kns50/index.aspx),and PubMed (http://www.ncbi.nlm.nih.gov/pubmed/) was performed to collect articles published between January 1990 and June 2009 with the key words "muscle exercise,apoptosis in the skeletal muscle" in Chinese and English,respectively.Articles highly correlated with current status and development of muscle exercise and apoptosis in the skeletal muscle were included:①studies on apoptosis in the skeletal muscle;②studies concerning exercise and apoptosis in the skeletal muscle;③studies involving gene regulation of exercise-induced apoptosis in the skeletal muscle;④studies on molecular mechanism of apoptosis in the skeletal muscle;⑤studies published in latest journal or similar field.Repetitive studies were excluded.RESULTS AND CONCLUSION:After exercise,apoptosis occurs in normal muscle or muscle under pathologic state.The apoptosis of skeletal muscle cells is similar to common cell apoptosis,including karyopyknosis,plasma membrane vacuole,cell organ shrinking,and apoptotic body formation.The apoptosis process is classified into three stages:initial,effector,and degradation stages.The increased apoptosis in the skeletal muscle is the primary reason for sports fatigue.Currently,studies of gene regulation of apoptosis in the skeletal muscle focus on apoptosis regulatory factor Bcl-2 protein,tumor necrosis α and death protease cysteine aspartase.The bcl-2 inhibits opening of mitochondrial permeability transition pore,suppresses proapoptosis protein release from mitochondria,and prevents mitochondrial membrane lipid peroxidation and mitochondrial matrix Ca~(2+) release to play anti-apoptotic effect.Tumor necrosis family plays an important role in initializing death factor and its receptor pathways,which depends on death ligand binding death receptor to activate cysteine aspartase and lead to cell apoptosis.The exploration of the relationship between exercise intensity and apoptosis and necrosis in skeletal muscle assists better understanding of the movement mechanism of exercise-induced fatigue and effectively reducing fatigue.