本文選題：力竭運(yùn)動 + 紅細(xì)胞��； 參考：《重慶大學(xué)》2014年博士論文

【摘要】：合理適度的運(yùn)動鍛煉能夠增強(qiáng)機(jī)體的免疫力，而力竭、缺氧等極端條件下的運(yùn)動通常伴隨著多種心血管疾病的增加，甚至猝死。已有的研究表明：運(yùn)動性休克、猝死等疾病往往伴隨著嚴(yán)重的心血管功能障礙的發(fā)生。其中，心室纖顫是導(dǎo)致運(yùn)動性猝死最常見的并發(fā)癥，而這種運(yùn)動誘導(dǎo)的致命性心律失常的發(fā)病機(jī)制仍不甚明確。一般認(rèn)為，動脈粥狀硬化患者心肌組織供血障礙或血栓形成及運(yùn)動性冠狀動脈痙攣是導(dǎo)致運(yùn)動性心肌局部供血不足，進(jìn)而誘發(fā)致命性心律紊亂的重要原因。然而，作為循環(huán)系統(tǒng)主要組分的紅細(xì)胞，其在不同運(yùn)動條件下對機(jī)體微循環(huán)暢通和組織供氧活動的影響仍有待研究。因此，研究不同運(yùn)動條件下RBC抗氧化、清除自由基能力的改變，自身受到氧化損傷程度的變化，以及氧化應(yīng)急條件下紅細(xì)胞力學(xué)性質(zhì)和攜氧功能的改變將對運(yùn)動誘發(fā)的休克、缺氧損傷、紅細(xì)胞凋亡等多種生理和病理現(xiàn)象的探索提供重要的理論依據(jù)。 機(jī)體在運(yùn)動過程中會產(chǎn)生大量的活性氧簇（ROS），這些ROS在組織生成后會迅速的釋放的血漿中。盡管紅細(xì)胞擁有非常完善的抗氧化機(jī)制，能夠迅速的清除來自胞內(nèi)和胞外的ROS。但是當(dāng)機(jī)體處于氧化應(yīng)激狀態(tài)時，持續(xù)、大量產(chǎn)生的ROS被釋放到血漿之中，使紅細(xì)胞的氧化-還原平衡被打破。本課題中，對不同運(yùn)動組大鼠紅細(xì)胞抗氧化指標(biāo)SOD、CAT和GSH檢測結(jié)果表明：力竭運(yùn)動后大鼠紅細(xì)胞抗氧化酶SOD和CAT的活性顯著增加，與此同時，胞內(nèi)主要的非酶類抗氧化物GSH含量出現(xiàn)顯著降低。這表明，力竭運(yùn)動使大鼠紅細(xì)胞抗氧化系統(tǒng)進(jìn)入應(yīng)急狀態(tài)，以抵御運(yùn)動誘導(dǎo)的自由基爆發(fā)。通過TBA法檢測膜脂質(zhì)TBARS水平，結(jié)果表明：力竭運(yùn)動導(dǎo)致大鼠紅細(xì)胞膜脂質(zhì)TBARS水平顯著升高。與此同時，胞內(nèi)高鐵血紅蛋白和膜結(jié)合高鐵血色原的含量也出現(xiàn)了顯著增加。紅細(xì)胞膜蛋白含有豐富的SH，它們對維系RBC膜上眾多酶類和功能蛋白的正常結(jié)構(gòu)功能起到重要作用。與對照組相比，力竭運(yùn)動后紅細(xì)胞膜蛋白SH含量也出現(xiàn)顯著下降。由此可見，力竭運(yùn)動誘導(dǎo)大鼠紅細(xì)胞出現(xiàn)嚴(yán)重的氧化應(yīng)激損傷。 在運(yùn)動引發(fā)的多種心腦血管疾病中，心肌、腦組織等局部供血不足被認(rèn)為是重要的并發(fā)癥。從紅細(xì)胞的角度看，紅細(xì)胞變形性和攜氧功能的維系對組織微循環(huán)暢通和有效攜氧起著重要的作用。本課題組，不同運(yùn)動條件下大鼠紅細(xì)胞變形能力和攜氧功能檢測分析結(jié)果表明：在力竭運(yùn)動過程中，由膜脂質(zhì)過氧化，，膜蛋白交聯(lián)等氧化應(yīng)激誘導(dǎo)的紅細(xì)胞損傷，紅細(xì)胞膜流動性下降，導(dǎo)致細(xì)胞變形能力降低。對RBC攜氧-釋氧熱力學(xué)和動力學(xué)曲線分析表明：在力竭運(yùn)動過程中，大鼠紅細(xì)胞攜氧熱力學(xué)曲線右移，P50值顯著升高；與此同時，紅細(xì)胞氧壓衰減曲線左移T50指標(biāo)都出現(xiàn)了顯著下降。這意味著，在力竭環(huán)境下大鼠紅細(xì)胞結(jié)合-釋放氧的胞內(nèi)環(huán)境以及相關(guān)的膜蛋白組分都受到了不同程度的影響或損傷。 紅細(xì)胞中以Band3蛋白為中心的蛋白復(fù)合體在維系紅細(xì)胞膜結(jié)構(gòu)完整性和穩(wěn)定性，以及調(diào)控紅細(xì)胞能量代謝和氣體轉(zhuǎn)運(yùn)的過程中都起到重要作用。這個大的Band3復(fù)合體的主要功能有：作為跨膜蛋白與骨架網(wǎng)路的連接樞紐，維持膜結(jié)構(gòu)的穩(wěn)定；與糖酵解酶類相互作用，調(diào)控糖代謝速率和途徑；與碳酸酐酶（CAII）等相互作用，形成代謝區(qū)室，形成以Band3為核心的O2/CO2交換中心。因此，為了進(jìn)一步探討力竭運(yùn)動誘導(dǎo)的紅細(xì)胞變形和攜氧功能障礙的分子機(jī)制，本文對運(yùn)動性氧化應(yīng)激反應(yīng)誘導(dǎo)的紅細(xì)胞膜Band3蛋白表達(dá)和分布情況及其調(diào)控的陰離子通道活性進(jìn)行了分析。Western Blotting和免疫熒光檢測的結(jié)果都表明：力竭運(yùn)動導(dǎo)致包括Band3蛋白在內(nèi)的膜蛋白交聯(lián)，導(dǎo)致紅細(xì)胞Band3蛋白結(jié)構(gòu)和功能性損傷。Band3蛋白的損傷將進(jìn)一步誘導(dǎo)紅細(xì)胞攜氧和變形能力的下降，成為運(yùn)動相關(guān)疾病的潛在致病因素。 為了進(jìn)一步探討力竭運(yùn)動誘導(dǎo)的紅細(xì)胞氧化損傷與運(yùn)動過程中血液氧含量的下降之間的關(guān)系。本文在體外條件下模擬不同氧分壓環(huán)境，并以次黃嘌呤/黃嘌呤氧化酶體系構(gòu)建了體外氧化模型。通過對不同氧分壓環(huán)境下紅細(xì)胞受氧化損傷程度和抗氧化能力的變化，初步探討了環(huán)境氧分壓與紅細(xì)胞氧化損傷的關(guān)系。結(jié)果表明：RBC氧化損傷和抗氧化力受環(huán)境氧分壓條件的影響。在不同氧分壓環(huán)境下，紅細(xì)胞血紅蛋白構(gòu)象在R態(tài)和T態(tài)之間的轉(zhuǎn)變會間接地導(dǎo)致胞內(nèi)糖代謝途徑的改變，從而對紅細(xì)胞氧化-還原代謝途徑產(chǎn)生影響。 論文還對力竭恢復(fù)階段大鼠紅細(xì)胞氧化應(yīng)激表現(xiàn)及紅細(xì)胞凋亡和再生過程進(jìn)行了初步的探討。結(jié)果表明，在力竭恢復(fù)初期大鼠紅細(xì)胞仍受到嚴(yán)重的氧化應(yīng)激損傷。伴隨著恢復(fù)時間的增加，受損傷嚴(yán)重的紅細(xì)胞逐漸衰老、凋亡。與此同時，體內(nèi)的造血系統(tǒng)被動員，產(chǎn)生大量的新鮮紅細(xì)胞以補(bǔ)充循環(huán)中受損傷清除的紅細(xì)胞。 綜上所述，本課題主要得出以下結(jié)論：力竭運(yùn)動過程中，機(jī)體進(jìn)入氧化應(yīng)激狀態(tài)。誘導(dǎo)大鼠紅細(xì)胞膜脂質(zhì)過氧化、膜蛋白聚簇化和血紅蛋白氧化在內(nèi)的氧化損傷。膜蛋白氧化損傷，尤其是Band3蛋白聚簇化和磷酸化程度的增加，導(dǎo)致力竭運(yùn)動后大鼠紅細(xì)胞攜氧功能和變形能力受到嚴(yán)重影響，使紅細(xì)胞在循環(huán)過程中氣體轉(zhuǎn)運(yùn)效率下降，成為組織局部供血不足等運(yùn)動性疾病的潛在致病因素。
[Abstract]:Reasonable exercise can enhance the immunity of the body, and the exercise under extreme conditions such as exhaustion and hypoxia is usually accompanied by the increase of a variety of cardiovascular diseases and even sudden death. The most common complication of sudden motor death, and the pathogenesis of the fatal arrhythmia induced by exercise is still not clear. It is generally believed that the blood supply disorder or thrombosis and motor coronary spasm in atherosclerotic patients lead to the insufficiency of the local blood supply of the motor myocardium, and then induce the fatal arrhythmia. However, as the main component of the circulation system, the influence of the red blood cells on the microcirculation and oxygen supply activities of the body under different sports conditions remains to be studied. Therefore, the study of the changes in the antioxidant capacity of RBC, the ability to scavenge free radicals, the changes in the degree of oxidative damage, and the oxidation emergency strip under different sports conditions are still to be studied. The changes in the mechanical properties and oxygen carrying functions of the red cells will provide important theoretical basis for the exploration of many physiological and pathological phenomena such as shock induced shock, hypoxia injury, erythrocyte apoptosis and so on.
While the body produces a large number of active oxygen clusters (ROS) during the process of movement, the ROS can be released rapidly after tissue formation. Although red cells have a very perfect antioxidant mechanism, it can quickly remove ROS. from both intracellular and extracellular, but when the body is in oxidative stress state, a large amount of ROS is released to the body. In the plasma, the oxidation-reduction balance of red blood cells was broken. In this study, the results of SOD, CAT and GSH of erythrocyte antioxidant indices of rats in different sports groups showed that the activity of antioxidant enzyme SOD and CAT increased significantly after exhaustive exercise, while the GSH content of the main non enzyme antioxidants in the cells decreased significantly. This shows that the exhaustion movement makes the rat erythrocyte antioxidant system enter the emergency state to resist the free radical outbreak induced by movement. The lipid TBARS level of the membrane is detected by TBA method. The results show that the level of lipid TBARS in the erythrocyte membrane of rats is significantly increased by the exhaustion movement. The original content also increased significantly. The erythrocyte membrane protein contains rich SH, which plays an important role in maintaining the normal structural functions of many enzymes and functional proteins on the RBC membrane. Compared with the control group, the content of the erythrocyte membrane protein SH after exhaustive exercise also decreased significantly. Severe oxidative stress damage.
In a variety of cardio cerebral vascular diseases caused by exercise, the insufficiency of local blood supply, such as myocardium and brain tissue, is considered as an important complication. From the point of view of the red cell, the deformability of red blood cells and the maintenance of oxygen carrying function play an important role in the smooth and effective oxygen carrying of tissue. The results of detection and analysis of capacity and oxygen carrying function showed that during the exhaustion movement, erythrocyte damage induced by lipid peroxidation, membrane protein crosslinking and other oxidative stress induced the decrease of erythrocyte membrane fluidity and the decrease of cell deformability. The analysis of the thermodynamics and kinetic curves of RBC oxygen carrying oxygen showed that during the exhaustion movement, it was large At the same time, the left shift T50 index of the red blood cell oxygen pressure attenuation curve decreased significantly. This means that the intracellular environment of erythrocyte binding oxygen release and the related membrane protein components in the exhausted environment were affected or damaged in varying degrees under the environment of exhaustion.
The Band3 protein complex in red cells plays an important role in maintaining the structural integrity and stability of the erythrocyte membrane, as well as in regulating the energy metabolism and gas transport of red blood cells. The major functions of the large Band3 complex are as the junction of the transmembrane protein and the skeleton network to maintain the membrane structure. Stability, interacting with glycolytic enzymes, regulating the rate and pathway of glycometabolism, interacting with carbonic anhydrase (CAII), forming a metabolic zone and forming a O2/CO2 exchange center with Band3 as the core. Therefore, in order to further explore the molecular mechanism of red cell deformation and oxygen carrying dysfunction induced by exhaustion movement, this article is on the movement oxidation. The expression and distribution of Band3 protein in erythrocyte membrane induced by stress reaction and its regulated anion channel activity were analyzed. The results of.Western Blotting and immunofluorescence detection showed that the exhaustion movement led to the membrane protein crosslinking including the Band3 protein, resulting in the structural and functional damage of the erythrocyte Band3 protein to.Band3 protein. The damage will further induce the decrease of oxygen carrying capacity and deformability of erythrocytes and become a potential pathogenic factor of sports related diseases.
In order to further investigate the relationship between the oxidative damage induced by exhaustive movement and the decrease of blood oxygen content during exercise, this paper simulates the different oxygen partial pressure environment under the conditions of in vitro, and constructs an in vitro oxidation model with the system of hypoxanthine / xanthine oxidase. The relationship between the environmental oxygen partial pressure and the oxidative damage of red cells was preliminarily discussed. The results showed that the oxidative damage and antioxidant capacity of RBC were affected by the conditions of environmental oxygen pressure. In different oxygen partial pressure conditions, the transformation of the erythrocyte hemoglobin conformation between the R state and the T state would indirectly lead to the intracellular sugar metabolism. The change of pathway will affect the redox pathway of RBC.
The results show that red blood cells still suffer severe oxidative stress in the early period of exhaustion recovery. With the increase of recovery time, the damaged red blood cells gradually aging and apoptosis. The hematopoietic system in the body is mobilized to produce a large amount of fresh red blood cells to supplement the damaged red cells in circulation.
To sum up, the following conclusions are drawn as follows: in the process of exhaustion movement, the body enters oxidative stress, induces lipid peroxidation in erythrocyte membrane, membrane protein clustering and oxidation of hemoglobin, and the oxidative damage of membrane protein, especially the increase of Band3 protein clustering and phosphorylation, resulting in exhaustion The function of oxygen carrying and deformability of red blood cells in rats is seriously affected, and the efficiency of gas transport in the cycle of erythrocytes is reduced, and it is a potential pathogenic factor of sports diseases such as the lack of local blood supply in the tissue.
【學(xué)位授予單位】：重慶大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2014
【分類號】：R87

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2 劉香江;重金屬銅和鎘(Cu和Cd)及乙酰甲胺磷對矛尾復(fù)蝦虎魚毒性效應(yīng)的研究[D];華中農(nóng)業(yè)大學(xué);2010年

3 徐小惠;優(yōu)秀散打運(yùn)動員十一運(yùn)決賽前體重控制、機(jī)能狀態(tài)和運(yùn)動能力的監(jiān)控研究[D];上海體育學(xué)院;2010年

4 李俊;上海武術(shù)隊(duì)重點(diǎn)運(yùn)動員賽前身體機(jī)能狀態(tài)監(jiān)控的研究[D];上海體育學(xué)院;2010年

5 柯可;多環(huán)芳烴—蒽對紫貽貝（Mytilus galloprpvincialis）生理生化效應(yīng)的研究[D];中國海洋大學(xué);2010年

6 張楊;地黃飲子對快速老化小鼠P8（SAMP8）定位導(dǎo)航學(xué)習(xí)記憶及氧化應(yīng)激的影響[D];黑龍江中醫(yī)藥大學(xué);2010年

7 田學(xué)忠;iNOS在肢體IR后關(guān)節(jié)損傷中的作用及組織芯片技術(shù)的初步應(yīng)用[D];泰山醫(yī)學(xué)院;2005年

8 馮菲;湘西香醋抗氧化及美容功效研究[D];中南林業(yè)科技大學(xué);2010年

9 王婧;利用小黃魚下腳料開發(fā)水產(chǎn)調(diào)味料及酶解液生理活性初步研究[D];浙江工商大學(xué);2011年

10 蓋春宇;硝苯地平的抗氧化活性研究[D];吉林大學(xué);2011年

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