本文選題：運(yùn)動(dòng)預(yù)適應(yīng) + 心臟保護(hù)��； 參考：《上海體育學(xué)院》2017年博士論文

【摘要】：研究目的:運(yùn)動(dòng)作為一個(gè)強(qiáng)度與負(fù)荷的刺激因素,極大地增加了心臟的耗氧量,導(dǎo)致心臟絕對(duì)或相對(duì)的缺氧。間歇大強(qiáng)度運(yùn)動(dòng)造成心臟反復(fù)短暫的絕對(duì)或相對(duì)缺血,與IP(ischemic preconditioning,IP)類(lèi)似,可以誘導(dǎo)心臟產(chǎn)生內(nèi)源性保護(hù),減輕隨后的急性應(yīng)激造成的心臟損傷,這種運(yùn)動(dòng)方式稱(chēng)為運(yùn)動(dòng)預(yù)適應(yīng)(exercise preconditioning,EP)。線粒體保護(hù)對(duì)心臟維持正常的生理狀態(tài)至關(guān)重要,同時(shí)又與氧化應(yīng)激聯(lián)系緊密。最近研究表明,細(xì)胞自噬與線粒體自噬在心肌中發(fā)揮重要的線粒體保護(hù)作用,且亦與氧化應(yīng)激聯(lián)系緊密。本研究以氧化應(yīng)激、線粒體、自噬三者為中軸線,結(jié)合EP的早、晚兩個(gè)保護(hù)期,以力竭運(yùn)動(dòng)作為損傷性應(yīng)激條件,利用自噬阻滯劑渥曼青霉素(wortmannin),并大量應(yīng)用蛋白線粒體轉(zhuǎn)位關(guān)系實(shí)驗(yàn),深入探討EP誘導(dǎo)的心臟保護(hù)中,氧化應(yīng)激、線粒體、自噬三者之間作用關(guān)系,理清心臟線粒體自噬發(fā)生機(jī)制。為EP心臟保護(hù)及機(jī)制研究提供新的理論和實(shí)驗(yàn)依據(jù)。研究方法:200只健康雄性SD大鼠隨機(jī)分為10組:C組,對(duì)照組;EE組,進(jìn)行一次大強(qiáng)度力竭跑臺(tái)運(yùn)動(dòng);EEP組,一次大強(qiáng)度間歇的跑臺(tái)運(yùn)動(dòng)建立EP模型,EP后0.5h取材;LEP組,EP建模后24h取材;EEP+EE組,EP后0.5h進(jìn)行力竭運(yùn)動(dòng);LEP+EE組,EP后24h進(jìn)行力竭運(yùn)動(dòng);W+EEP組,EP前0.5h腹腔注射渥曼青霉素,EP后0.5取材;W+LEP組,阻滯劑注射如W+EEP組,EP后24h取材;W+EEP+EE組,阻滯劑注射同前,EP后0.5h進(jìn)行力竭運(yùn)動(dòng);W+LEP+EE組,阻滯劑注射同前,EP后24h進(jìn)行力竭運(yùn)動(dòng)。應(yīng)用免疫熒光發(fā)光法檢測(cè)大鼠血漿心肌肌鈣蛋白I(c Tn I)水平評(píng)價(jià)心肌損傷;應(yīng)用蘇木素堿性復(fù)紅苦味酸染色(HBFP staining)觀察和評(píng)估心肌缺血缺氧程度;應(yīng)用透射電鏡觀察心肌超微結(jié)構(gòu)改變,著重觀察線粒體和自噬體;應(yīng)用分光光度法檢測(cè)大鼠心肌丙二醛(MDA)、過(guò)氧化氫(H2O2)、錳超氧化物歧化酶(Mn SOD)和總超氧化物歧化酶活性,以及免疫印跡法檢測(cè)Mn SOD含量,評(píng)價(jià)氧化應(yīng)激程度;應(yīng)用Phos-tag法檢測(cè)電壓門(mén)控陰離子通道1(VDAC1)磷酸化水平,評(píng)價(jià)線粒體滲透性轉(zhuǎn)換孔道(m PTP)抑制程度;應(yīng)用線粒體提取結(jié)合免疫印跡法檢測(cè),細(xì)胞色素C(Cyt-c)、自噬受體p62、線粒體自噬蛋白Parkin和Bnip3,評(píng)價(jià)上述蛋白在胞漿和線粒體的含量變化;應(yīng)用免疫印跡法檢測(cè)自噬關(guān)鍵蛋白Beclin1、Bcl-2、LC3I、LC3II水平,結(jié)合Beclin1/Bcl-2、LC3II/LC3I比值計(jì)算,評(píng)價(jià)細(xì)胞自噬水平和性質(zhì);應(yīng)用組織免疫熒光雙標(biāo)法結(jié)合激光共聚焦技術(shù),檢測(cè)LC3對(duì)線粒體內(nèi)膜蛋白COX4/1、Parkin對(duì)線粒體外膜轉(zhuǎn)運(yùn)酶TOM70、Bnip3對(duì)TOM20的轉(zhuǎn)位水平和上述六種蛋白的熒光表達(dá)量和分布。通過(guò)上述指標(biāo)深入揭示氧化應(yīng)激與線粒體自噬在ep誘導(dǎo)心臟保護(hù)中的作用和機(jī)制。研究結(jié)果:(1)與c組相比,ee組心肌損傷標(biāo)志物血漿ctni水平、hbfp染色缺血缺氧程度均有顯著升高,損傷性超微結(jié)構(gòu)改變明顯;eep組和lep組無(wú)損傷性改變。與ee組相比,eep+ee和lep+ee組,血漿ctni水平降低、缺血缺氧和超微結(jié)構(gòu)改變均有減輕。與eep+ee組相比,w+eep+ee組血漿ctni水平略有降低,但缺血缺氧未見(jiàn)改變且有升高趨勢(shì),線粒體肥大明顯。與lep+ee組相比,w+lep+ee組血漿ctni和缺血缺氧均有升高,線粒體損傷明顯。(2)與c組相比,ee組氧化應(yīng)激損傷產(chǎn)物mda顯著升高,總sod活性降低,氧化應(yīng)激損傷明顯,但h2o2、mnsod活性和含量無(wú)變化;eep組和lep組,mnsod、總sod活性均有升高,無(wú)mda升高和mnsod含量變化,eep組h2o2顯著減低。與ee組相比,eep+ee組mda明顯下降,h2o2、總sod活性明顯升高;lep+ee組總sod活性升高,但eep+ee組和lep+ee組sod酶活性?xún)蓴?shù)據(jù)均分別較之eep組和lep組有明顯下降。與eep+ee組相比,w+eep+ee組mda和mnsod活性均明顯增高。與lep+ee組相比,w+lep+ee組h2o2顯著升高。(3)與c組相比,ee組和eep+ee組,抑制mptp開(kāi)放的vdac1磷酸化水平顯著升高。與ee組相比,lep+ee組、w+eep+ee組、w+lep+ee組vdac1磷酸化水平降低。與eep+ee組相比,w+eep+ee組vdac1磷酸化水平顯著降低,線粒體cyt-c泄漏至胞漿顯著增高。(4)與c組相比,ee組lc3ii和lc3ii/lc3i比值顯著升高;eep組lc3ii/lc3i比值升高;eep+ee組lc3ii和beclin1含量升高提示細(xì)胞自噬增強(qiáng);w+lep組lc3ii、lc3ii/lc3i比值、beclin1/bcl-2比值升高凋亡性自噬水平增高;w+eep+ee組和w+lep+ee組兩種比值均升高自噬為凋亡性。與ee組相比,lep+ee組lc3ii和lc3ii/lc3i顯著降低,細(xì)胞自噬水平較低;w+eep+ee組beclin1升高。(5)與c組相比,ee組lc3轉(zhuǎn)位線粒體cox4/1百分比、線粒體p62降低;eep組lc3轉(zhuǎn)位顯著降低;w+lep組cox4/1熒光強(qiáng)度降低。與ee組相比,eep+ee組lc3轉(zhuǎn)位程度、lc3熒光強(qiáng)度、胞漿p62均顯著增高;lep+ee組lc3轉(zhuǎn)位程度升高、lc3和cox4/1熒光強(qiáng)度降低;w+eep+ee組lc3轉(zhuǎn)位程度降低,胞漿和線粒體p62均升高;w+lep+ee組lc3轉(zhuǎn)位、線粒體p62升高,lc3、cox4/1熒光強(qiáng)度顯著降低。與eep+ee組相比,w+eep+ee組lc3熒光強(qiáng)度顯著降低。(6)與c組相比,ee組線粒體parkin、parkin轉(zhuǎn)位tom70程度、parkin和tom70熒光強(qiáng)度顯著降低,胞漿和線粒體bnip3、bnip3轉(zhuǎn)位tom20程度、bnip3熒光強(qiáng)度均顯著升高,tom20熒光強(qiáng)度無(wú)變化;eep組parkin轉(zhuǎn)位、tom70和tom20熒光強(qiáng)度顯著降低,胞漿和線粒體bnip3表達(dá)量升高;lep組bnip3轉(zhuǎn)位程度、胞漿和線粒體bnip3水平顯著增高;w+eep組、w+lep組分別與eep組和lep組在線粒體自噬指標(biāo)上接近。與ee組相比,eep+ee組線粒體parkin和parkin轉(zhuǎn)位,parkin、TOM70、Bnip3熒光強(qiáng)度均顯著升高,胞漿和線粒體Bnip3水平和EE組接近;LEP+EE組線粒體Parkin含量、Parkin轉(zhuǎn)位和TOM70熒光強(qiáng)度升高,Bnip3相關(guān)數(shù)據(jù)均顯著下降;W+EEP+EE組Parkin相關(guān)數(shù)據(jù)均有顯著升高,但Parkin轉(zhuǎn)位程度顯著低于EEP+EE組,胞漿Bnip3和TOM20顯著升高;W+LEP+EE組Parkin轉(zhuǎn)位和熒光強(qiáng)度升高。與EEP+EE組相比,W+EEP+EE組Parkin熒光強(qiáng)度顯著升高,Bnip3和TOM20熒光強(qiáng)度顯著降低。與LEP+EE組相比,W+LEP+EE組Parkin轉(zhuǎn)位顯著降低,Bnip3轉(zhuǎn)位、Bnip3和TOM20熒光強(qiáng)度顯著升高。研究結(jié)論:(1)一次力竭運(yùn)動(dòng)造成明顯的心肌損傷、缺血缺氧、超微結(jié)構(gòu)損傷以及氧化應(yīng)激損傷。但線粒體本身?yè)p傷并不嚴(yán)重,也無(wú)法引起凋亡�？赡芡ㄟ^(guò)抑制m PTP開(kāi)放,和增強(qiáng)線粒體分裂以誘導(dǎo)Bnip3依賴(lài)的線粒體自噬參與有限的線粒體保護(hù)。(2)EP是無(wú)損傷的運(yùn)動(dòng)方式,可以誘導(dǎo)SOD酶活性升高,并降低H2O2水平,提供心肌適應(yīng)性。在EP的早期保護(hù)時(shí)相,m PTP被抑制,H2O2誘導(dǎo)了修復(fù)性線粒體自噬水平升高,Parkin和Bnip3均有參與,但Bnip3可能作用更大。在EP的晚期保護(hù)時(shí)相,Parkin介導(dǎo)的修復(fù)性自噬占到了主導(dǎo)作用。(3)自噬阻滯劑wortmannin對(duì)EP誘導(dǎo)的線粒體保護(hù)產(chǎn)生負(fù)面影響,但不會(huì)引起EP本身的損傷加劇。在EP早期保護(hù)時(shí)相,被阻滯的細(xì)胞自噬引起細(xì)胞一型前凋亡表型上升,使線粒體保護(hù)喪失。在EP的晚期保護(hù)時(shí)相,反而激活了凋亡性自噬,使心肌保護(hù)喪失。
[Abstract]:Research purposes: exercise, as a stimulus for intensity and load, greatly increases the oxygen consumption of the heart and leads to absolute or relative hypoxia. Intermittent large intensity exercise causes repeated absolute or relative ischemia of the heart, similar to IP (ischemic preconditioning, IP), which can induce endogenous protection in the heart and reduce the following. The heart damage caused by acute stress, which is called exercise preconditioning (EP). Mitochondrial protection is vital to the normal physiological state of the heart, and is closely associated with oxidative stress. Recent studies have shown that autophagy and mitochondrial autophagy play an important role in mitochondrial protection in the heart. This study used oxidative stress, mitochondria and autophagy three as the central axis, combined with the early and late two protective periods of EP, the exhaustive exercise as a damaging stress condition, the use of autophagic blocker walman penicillin (wortmannin), and a large amount of application of protein mitochondrial translocation experiments, to further explore the induction of EP. In the heart protection, the relationship between oxidative stress, mitochondria, autophagy and the mechanism of autophagy between three groups, clarify the mechanism of cardiac mitochondrial autophagy. Provide new theoretical and experimental basis for EP heart protection and mechanism research. Research methods: 200 healthy male SD rats were randomly divided into 10 groups: group C, group EE, a large intensity exhausted running table exercise; EEP Group, a EP model was established for a large and intermittent running platform, and 0.5h was obtained after EP; LEP group, 24h after EP modeling; EEP+EE group, EP after 0.5h carried out exhaustion movement; LEP+EE group, EP 24h carried out exhaustion movement; The blockers were injected before the same time and 0.5h was exhausted after EP; group W+LEP+EE, blockers were injected before the same time, and 24h was exhausted after EP. The level of cardiac troponin I (C Tn I) in rat plasma was evaluated by immunofluorescence. The myocardial ischemia and hypoxia was observed and evaluated by hematoxylin basic complex red bitteric acid staining (HBFP staining). The ultrastructural changes of myocardium were observed with transmission electron microscope, and mitochondria and autophagic were observed emphatically. The activity of MDA, H2O2, Mn SOD and total superoxide dismutase were detected by spectrophotometry, and the content of Mn SOD was detected by Western blot, and the degree of oxidative stress was evaluated. The level of phosphorylation of voltage gated anion channel 1 (VDAC1) was detected by Phos-tag method, and the inhibition degree of mitochondrial permeability transition channel (m PTP) was evaluated. Mitochondria extraction combined with immunoblotting, cytochrome C (Cyt-c), autophagic receptor p62, mitochondria autophagic egg white Parkin and Bnip3 were used to evaluate the content of these proteins in cytoplasm and mitochondria. The key proteins of autophagy Beclin1, Bcl-2, LC3I, LC3II were detected by Western blot, and the level and properties of autophagy were evaluated by the ratio of Beclin1/Bcl-2 and LC3II/LC3I. The tissue immunofluorescence double labeling method combined with laser confocal technique was used to detect the endometrial protein COX4/1 of LC3 and Parkin to the mitochondrial membrane transporter TOM70. Bnip3's transposition level of TOM20 and the fluorescence expression and distribution of the above six proteins. Through the above indicators, the role and mechanism of oxidative stress and mitochondrial autophagy in EP induced cardiac protection were revealed. (1) compared with the C group, the level of plasma cTnI in the myocardial damage markers in EE group and the degree of ischemic anoxia by HBFP staining were significantly increased. In the group eep and the group LEP, the level of plasma cTnI decreased and the ischemic anoxia and ultrastructural changes were reduced. Compared with the group of eep+ee, the level of cTnI decreased slightly in the group of w+eep+ee, but in the group of w+eep+ee, the blood oxygen deficiency was not changed and increased, and the mitochondrial fertilizer Daming was found. Compared with the lep+ee group, the plasma cTnI and ischemic anoxia in the w+lep+ee group were increased and the mitochondrial damage was obvious. (2) compared with the C group, the oxidative stress damage product MDA was significantly increased in the EE group, the total SOD activity was reduced, the oxidative stress was obviously damaged, but the activity and content of MnSOD were not changed, and the EEP and LEP groups, MnSOD, no higher activity increased. With the change of MnSOD content, H2O2 in group eep decreased significantly. Compared with group EE, MDA decreased significantly in group eep+ee, H2O2, total SOD activity increased obviously, and the total SOD activity of lep+ee group increased, but the two data of eep+ee group and lep+ee group decreased significantly. Compared with group lep+ee, H2O2 was significantly higher in group w+lep+ee. (3) the phosphorylation level of Vdac1 in group EE and eep+ee group was significantly higher than that in group EE and eep+ee group. Compared with group EE, the phosphorylation level of lep+ee, w+eep+ee, and w+lep+ee groups decreased. (4) the ratio of lc3ii to lc3ii/lc3i in group EE was significantly higher than that in group C, and the ratio of lc3ii/lc3i in eep group increased. The increase of lc3ii and Beclin1 content in eep+ee group suggested that the cell autophagy increased, w+lep lc3ii, lc3ii/lc3i ratio, increase of apoptotic autophagy increased, and the ratio of two kinds of autophagy increased in both group and group. Compared with group EE, lc3ii and lc3ii/lc3i decreased significantly in group lep+ee, the level of autophagy was lower and Beclin1 in w+eep+ee group increased. (5) compared with the C group, the percentage of cox4/1 in the LC3 transposition of EE group was lower than that in the C group. Fluorescence intensity, cytoplasmic p62 increased significantly, LC3 transposition in lep+ee group increased, LC3 and cox4/1 fluorescence intensity decreased, LC3 transposition in w+eep+ee group decreased, cytoplasm and mitochondrial p62 increased, w+lep+ee group LC3 transposition, mitochondria p62 increased, LC3, fluorescence intensity decreased significantly (6 Compared with the C group, the mitochondrial Parkin, parkin transposition tom70, parkin and tom70 fluorescence intensity decreased significantly, the cytoplasm and mitochondrial BNIP3, the BNIP3 transposition Tom20 degree, BNIP3 fluorescence intensity increased significantly, and the Tom20 fluorescence intensity was not changed. The level of BNIP3 transposition and the level of cytoplasm and mitochondrial BNIP3 increased significantly in group LEP, and in group w+eep, group w+lep was close to the mitochondrial autophagy index in group eep and LEP group. Compared with group EE, the mitochondrial parkin and parkin transposition of eep+ee group was significantly higher than that of EE group, and the level of cytoplasm and mitochondria was close to that of the group. Mitochondrial Parkin content, Parkin transposition and TOM70 fluorescence intensity increased, and Bnip3 related data were significantly decreased, and Parkin related data in W+EEP+EE group were significantly increased, but the degree of Parkin transposition was significantly lower than that in EEP+EE group, and Bnip3 and TOM20 increased significantly in the cytoplasm; W+LEP+EE group Parkin transposition and fluorescence intensity increased. The fluorescence intensity of Bnip3 and TOM20 decreased significantly. Compared with the LEP+EE group, the Parkin transposition of the W+LEP+EE group decreased significantly, the Bnip3 transposition, and the fluorescence intensity of Bnip3 and TOM20 increased significantly. (1) the first exhaustive exercise resulted in obvious myocardial injury, ischemic oxygen deficiency, ultrastructural damage and oxidative stress injury. Its own damage is not serious, nor can it cause apoptosis. It may be possible by inhibiting m PTP opening and enhancing mitochondrial division to induce Bnip3 dependent mitochondrial autophagy to participate in limited mitochondrial protection. (2) EP is a noninvasive mode of exercise that can induce the increase of SOD enzyme activity and reduce the level of H2O2 and provide myocardial adaptability. In the early protection of EP Phase, m PTP was inhibited, H2O2 induced elevated mitochondrial autophagy, Parkin and Bnip3 were involved, but Bnip3 may play a greater role. In the late protection phase of EP, Parkin mediated repair autophagy dominated the role. (3) autophagic blocker wortmannin has a negative effect on EP induced mitochondrial protection, but does not cause EP Ben. The damage to the body is aggravated. In the early protection of EP, the blocked cell autophagy caused the apoptotic phenotype of the cell to rise, causing the loss of mitochondrial protection. In the late EP protection phase, the apoptotic autophagy was activated and the myocardial protection was lost.
【學(xué)位授予單位】：上海體育學(xué)院
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2017
【分類(lèi)號(hào)】：G804.2

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7 黃彬;運(yùn)動(dòng)、機(jī)體的抗氧化能力與衰老[J];南京體育學(xué)院學(xué)報(bào)(自然科學(xué)版);2003年04期

8 肖曉玲;黃文英;吳韜;;桑黃粗多糖對(duì)被動(dòng)吸煙小鼠肝臟氧化應(yīng)激實(shí)驗(yàn)研究[J];體育科技;2013年03期

9 張金梁;;游泳訓(xùn)練改善心梗造成的心肌氧化應(yīng)激:激活PI3K-AKt信號(hào)級(jí)聯(lián)的核心作用[J];山東體育學(xué)院學(xué)報(bào);2012年05期

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7 熊昌彪;氧化應(yīng)激研究與中醫(yī)治未病“不謀而合”[N];中國(guó)醫(yī)藥報(bào);2008年

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