【摘要】： 本實(shí)驗(yàn)室設(shè)計(jì)并合成的含有組氨酸殘基的單體亞血紅素六肽(Deuterohaemin-Ala-His-Thr-Val-Glu-Lys, DhHP-6),具有較高的抗壞血酸過(guò)氧化物酶活性,活性可達(dá)3.9x103U·μmol-1(天然微過(guò)氧化物酶MP-11的93%),是一種新的過(guò)氧化物酶模擬物,其分子量小,可進(jìn)入心肌細(xì)胞;它能類似人體自然過(guò)程,有效地清除體內(nèi)的過(guò)氧化物、超氧離子和自由基。 隨著多種血管再通技術(shù)在臨床的廣泛應(yīng)用,心肌缺血再灌注(IR)損傷已越來(lái)越受到廣大科研工作者的重視,但其作用機(jī)制至今尚未完全清楚。本課題采用培養(yǎng)的HeLa細(xì)胞和H9C2細(xì)胞建立缺氧再給氧(HR)損傷模型,從細(xì)胞水平研究DhHP-6對(duì)培養(yǎng)細(xì)胞缺氧再給氧損傷的保護(hù)作用,并對(duì)其作用機(jī)制進(jìn)行初步探討。通過(guò)對(duì)培養(yǎng)的HeLa細(xì)胞和H9C2細(xì)胞的形態(tài)觀察,細(xì)胞存活率的測(cè)定,Ca++-ATPase活力的測(cè)定,LDH活力的測(cè)定,細(xì)胞活力的測(cè)定,AO/EB雙染以及H9C2細(xì)胞SOD活力的測(cè)定和MDA含量的測(cè)定,證明DhHP-6具有減輕細(xì)胞缺氧再給氧損傷的作用,其機(jī)制與對(duì)抗氧自由基、降低細(xì)胞內(nèi)[Ca2+]有關(guān)。
[Abstract]:The monomer heme hexapeptide (Deuterohaemin-Ala-His-Thr-Val-Glu-Lys, DhHP-6) with histidine residue was designed and synthesized in our laboratory. It has high activity of ascorbic acid peroxidase (ascorbic acid peroxidase). The activity of 3.9x103U 渭 mol-1 (93% of the natural microperoxidase MP-11) is a new peroxidase mimic, and its molecular weight is small and it can enter cardiomyocytes. It can be similar to the natural process of the human body, effectively scavenging the body of peroxides, superoxide ions and free radicals. With the wide application of various vascular recanalization techniques, myocardial ischemia-reperfusion (IR) injury has been paid more and more attention by researchers, but its mechanism has not been fully understood. In this study, HeLa cells and H9C2 cells were used to establish the model of (HR) injury induced by hypoxia and reoxygenation. The protective effect of DhHP-6 on hypoxia and reoxygenation injury of cultured cells was studied at the cell level, and the mechanism was discussed. The morphology of cultured HeLa cells and H9C2 cells, cell survival rate, Ca ATPase activity, LDH activity, cell viability, AO/EB double staining, SOD activity of H9C2 cells and MDA content were measured. It is proved that DhHP-6 can alleviate the damage of hypoxia and reoxygenation, and its mechanism is related to the inhibition of oxygen free radical and the decrease of intracellular [Ca2].
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2008
【分類號(hào)】：R341

【引證文獻(xiàn)】

相關(guān)碩士學(xué)位論文 前3條

1 朱媛媛;亞鐵血紅素的酶法制備及功能特性研究[D];吉林大學(xué);2011年

2 張超;次血紅素六肽抗納米金介導(dǎo)的線蟲(chóng)熱損傷作用研究[D];吉林大學(xué);2010年

3 馮建宇;鈣通道阻斷劑對(duì)低鉀狀態(tài)下大鼠缺血—再灌注心功能恢復(fù)的作用觀察[D];第四軍醫(yī)大學(xué);2012年

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本文編號(hào)：2372037