本文關(guān)鍵詞：氧化低密度脂蛋白對紅細(xì)胞的損傷　出處：《重慶大學(xué)》2005年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 氧化損傷 紅細(xì)胞膜蛋白 膜粘彈性 動脈粥樣硬化

【摘要】：血液流變學(xué)研究正朝著細(xì)胞水平和分子水平發(fā)展,在細(xì)胞和分子水平上更深入地研究引起紅細(xì)胞力學(xué)特性變化及整個血液流變學(xué)特性變化的分子生物學(xué)機制,有助于從根本上認(rèn)識紅細(xì)胞變形的生理和臨床意義,為許多與紅細(xì)胞流變學(xué)相關(guān)的疾病的基礎(chǔ)病理研究和臨床研究提供重要的依據(jù)。 生物學(xué)和醫(yī)學(xué)界一般認(rèn)為,低密度脂蛋白(LDL)被氧化修飾為氧化低密度脂蛋白(Ox—LDL)后, 能損傷動脈內(nèi)皮細(xì)胞,損傷的動脈內(nèi)皮細(xì)胞就會轉(zhuǎn)化為泡沫細(xì)胞, 進(jìn)而形成AS 病灶,這說明低密度脂蛋白促進(jìn)AS 的發(fā)生和發(fā)展;但生物學(xué)和醫(yī)學(xué)界就Ox—LDL 對紅細(xì)胞的損傷了解甚少。通過大量的實驗研究證明:紅細(xì)胞主要的力學(xué)性質(zhì)表現(xiàn)為紅細(xì)胞膜的粘彈性,紅細(xì)胞膜的粘彈性的變化與生物體內(nèi)普遍存在的,膜蛋白的氧化損傷與氧自由基反應(yīng)機制間存在明確的相關(guān)性,從而說明紅細(xì)胞膜的氧化損傷是導(dǎo)致紅細(xì)胞膜力學(xué)性質(zhì)變化的分子生物學(xué)機制。(可能來自不同的病理或生理原因,但都產(chǎn)生氧自由基損傷) 在本研究工作中,檢索查閱了相關(guān)的文獻(xiàn)資料,應(yīng)用了細(xì)胞流變學(xué)的基本原理和實驗方法,學(xué)習(xí)了Chien 的關(guān)于紅細(xì)胞膜(本構(gòu)關(guān)系)“半球帽子模型”,通過該模型來研究膜蛋白氧化損傷對膜變形的動力學(xué)過程的影響;結(jié)合分子生物學(xué)的理論和生化分析方法,運用分子生物學(xué)技術(shù),通過SDS-PAGE 電泳,表明氧化損傷的膜蛋白中出現(xiàn)分子量高于Spectrin的新譜帶HMB,其結(jié)果將限制膜蛋白的空間構(gòu)象變化和共振自由度,最終導(dǎo)致膜彈性系數(shù)和膜粘性系數(shù)的變化。本文系統(tǒng)地研究了紅細(xì)胞膜蛋白的氧化損傷對紅細(xì)胞膜粘彈性的影響和膜蛋白組成的改變。 通過本文的研究,我們可以認(rèn)為:Ox—LDL 對紅細(xì)胞的損傷主要表現(xiàn)為紅細(xì)胞膜的損傷即膜蛋白組成的改變,紅細(xì)胞膜損傷后,使紅細(xì)胞的變形性降低及攜氧和釋氧能力的下降,紅細(xì)胞的變形性降低使得血液粘性增加,血流速度減慢,導(dǎo)致內(nèi)皮細(xì)胞受損;紅細(xì)胞變形性減退意味著穩(wěn)定性下降,紅細(xì)胞溶解釋放的二磷酸腺苷引起血小板活化,參與動脈粥樣硬化的發(fā)展。因此,Ox—LDL 對紅細(xì)胞的損傷使紅細(xì)胞變形性降低是動脈粥樣硬化繼發(fā)性改變,并且參與動脈粥樣硬化的發(fā)展。
[Abstract]:The research of hemorheology is developing towards the cellular and molecular level, and the molecular biological mechanism that causes the change of the erythrocyte mechanical properties and the whole hemorheological characteristics is studied more deeply at the cellular and molecular level. It is helpful to understand the physiological and clinical significance of erythrocyte deformability and provide important basis for the basic pathological and clinical study of many diseases related to erythrocyte rheology. It is generally believed in biology and medicine that low density lipoprotein (LDL) can damage arterial endothelial cells after oxidative modification to oxidize LDL. The injured arterial endothelial cells will be transformed into foam cells, and then form as lesions, which indicates that LDL promotes the development and development of as. However, biology and medicine know little about the damage of Ox-LDL to erythrocyte. Through a large number of experimental studies, it has been proved that the main mechanical properties of erythrocyte are viscoelasticity of erythrocyte membrane. The change of viscoelasticity of erythrocyte membrane is common in organism. There is a clear correlation between the oxidative damage of membrane protein and the mechanism of oxygen free radical reaction. Therefore, the oxidative damage of erythrocyte membrane is the molecular biological mechanism that causes the change of the mechanical properties of erythrocyte membrane. (may come from different pathological or physiological reasons, but all produce oxygen free radical damage) In this study, we searched the relevant literature and applied the basic principles and experimental methods of cell rheology. The hemispherical hat model of erythrocyte membrane (constitutive relation) proposed by Chien was studied to study the effect of oxidative damage of membrane protein on the dynamic process of membrane deformation. Combined with the theory of molecular biology and biochemical analysis methods, using molecular biology technology, SDS-PAGE electrophoresis. The results showed that a new band with molecular weight higher than Spectrin appeared in the membrane proteins with oxidative damage, which would limit the spatial conformation change and resonance degree of freedom of the membrane proteins. The effects of oxidative damage of erythrocyte membrane protein on the membrane viscoelasticity and the composition of membrane protein were systematically studied. Through the research in this paper, we can conclude that the damage to red blood cells caused by w / Ox-LDL is mainly the damage of erythrocyte membrane, that is, the change of membrane protein composition, after the damage of erythrocyte membrane. The deformability of erythrocytes and the ability of oxygen delivery and oxygen release were decreased, and the deformability of erythrocytes increased blood viscosity and blood flow velocity, resulting in endothelial cell damage. Decreased erythrocyte deformability means a decrease in stability. Adenosine diphosphate, which is released from erythrocytic dissolution, causes platelet activation and is involved in the development of atherosclerosis. The decrease of erythrocyte deformability caused by Ox-LDL injury is a secondary change of atherosclerosis and is involved in the development of atherosclerosis.
【學(xué)位授予單位】：重慶大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2005
【分類號】：R329.2

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