發(fā)布時(shí)間：2018-06-13 18:11

  本文選題：光散射 + 晶狀體��； 參考：《山東大學(xué)》2010年博士論文

【摘要】：臨床意義 白內(nèi)障是世界首位致盲眼病,晶狀體的氧化損傷是白內(nèi)障形成的主要機(jī)制。大量臨床和流行病學(xué)研究已經(jīng)證實(shí),紫外線輻射(ultraviolet radiation, UVR)是人類白內(nèi)障形成和發(fā)展最重要的危險(xiǎn)因素之一。近年來,氣候污染造成的大氣臭氧層破壞更增加了紫外線對(duì)地球的輻射,不可避免地危害人類健康,大大增加了白內(nèi)障形成的危害性。同時(shí),隨著世界人口的不斷增長和人口老齡化的加劇,白內(nèi)障的發(fā)病率會(huì)持續(xù)升高。白內(nèi)障造成的公共健康問題和所帶來的經(jīng)濟(jì)負(fù)擔(dān)日益加重,對(duì)我們研究紫外線輻射導(dǎo)致白內(nèi)障形成和發(fā)展機(jī)制、探討晶狀體內(nèi)自身抗氧化防御體系的保護(hù)作用提出了新的要求；同時(shí)對(duì)研究和開發(fā)非手術(shù)性預(yù)防和延遲白內(nèi)障的新方法提出了更高的目標(biāo)。因此WHO提出防護(hù)紫外線輻射,研究開發(fā)低成本的抗氧化劑是預(yù)防和延遲白內(nèi)障的首要目標(biāo)。 本課題的研究目的：通過建立近閾值量紫外線(UVR-300nm)誘導(dǎo)的大鼠白內(nèi)障模型,采用測(cè)量晶狀體光散射強(qiáng)度的方法,對(duì)紫外線照射后晶狀體的混濁程度進(jìn)行定量研究和動(dòng)態(tài)觀察；分光光度法對(duì)紫外線照射后不同時(shí)間晶狀體內(nèi)谷胱甘肽氧化還原體系中的相應(yīng)生化指標(biāo)進(jìn)行定量分析和動(dòng)態(tài)研究,進(jìn)一步探討紫外線導(dǎo)致白內(nèi)障形成和發(fā)展的機(jī)制。同時(shí)研究和探討抗氧化劑α-生育酚(維生素E)對(duì)紫外線誘導(dǎo)大鼠白內(nèi)障的保護(hù)作用與其劑量之間的量效關(guān)系；以及α-生育酚對(duì)紫外線照射后晶狀體內(nèi)谷胱甘肽氧化還原體系的影響和相互作用。為今后進(jìn)行α-生育酚防護(hù)紫外線輻射白內(nèi)障的研究提供詳實(shí)的實(shí)驗(yàn)數(shù)據(jù),更好地開發(fā)和利用維生素E的重要生物功能,為臨床合理應(yīng)用維生素E預(yù)防和延遲白內(nèi)障的發(fā)展提供可循的實(shí)驗(yàn)依據(jù)。 實(shí)驗(yàn)一： 紫外線誘導(dǎo)的大鼠白內(nèi)障晶狀體內(nèi)谷胱甘肽氧化還原平衡體系的變化 目的：觀察近閾值量紫外線誘導(dǎo)的大鼠白內(nèi)障隨時(shí)間變化的特點(diǎn)；研究紫外線照射后不同時(shí)間晶狀體內(nèi)谷胱甘肽氧化還原平衡體系的動(dòng)態(tài)變化；探討紫外線誘導(dǎo)白內(nèi)障形成和發(fā)展的機(jī)制。 方法：40只6周齡的albino Spraque Dawley雌性大鼠隨機(jī)分為4組,每組10只大鼠,實(shí)驗(yàn)組大鼠單側(cè)眼行紫外線照射(UVR-300 nm,8 kJ/m2)15分鐘；另一組未行紫外線照射的大鼠作為正常對(duì)照組。3個(gè)實(shí)驗(yàn)組大鼠分別于紫外線照射后1、3和7天處死,摘除雙側(cè)眼球,分離晶狀體,測(cè)量晶狀體光散射強(qiáng)度,定量分析晶狀體混濁度,暗背景光晶狀體照像,分光光度法測(cè)定晶狀體內(nèi)還原型(reduced glutathione, GSH)和氧化型(oxidized glutathione, GSSG)谷胱甘肽濃度及谷胱甘肽還原酶(glutathione reductase, GR)和谷胱甘肽過氧化物酶(glutathione peroxidase, GPx)的活性。正常對(duì)照組大鼠,提供大鼠正常晶狀體各項(xiàng)實(shí)驗(yàn)參數(shù)的基線值。紫外線照射眼晶狀體與對(duì)側(cè)未照射眼晶狀體各項(xiàng)實(shí)驗(yàn)參數(shù)差值的平均值作為統(tǒng)計(jì)學(xué)分析的原始數(shù)據(jù)。 結(jié)果：紫外線照射眼的晶狀體混濁程度隨紫外線照射后時(shí)間的增加而逐漸加重；而正常對(duì)照組大鼠晶狀體和實(shí)驗(yàn)組大鼠的對(duì)側(cè)未照射眼晶狀體,均未發(fā)現(xiàn)明顯混濁；紫外線照射眼與對(duì)側(cè)未照射眼晶狀體光散射強(qiáng)度的差值,與正常對(duì)照組大鼠的晶狀體比較,差異有統(tǒng)計(jì)學(xué)意義。紫外線照射后第1天,晶狀體內(nèi)GSH濃度出現(xiàn)一過性升高,隨后GSH濃度隨照射后時(shí)間的增加而逐漸下降,至紫外線照射后第7天GSH濃度仍未恢復(fù)到正常水平；紫外線照射后第1天,紫外線照射眼與對(duì)側(cè)未照射眼晶狀體GSH濃度的差值,與紫外線照射后第3天和第7天比較,差異有統(tǒng)計(jì)學(xué)意義。紫外線照射后第1天,晶狀體內(nèi)GPx活性出現(xiàn)一過性增強(qiáng),隨后GPx活性隨照射后時(shí)間的增加而逐漸下降,至紫外線照射后第7天GPx活性已恢復(fù)到正常水平；紫外線照射后第1天,紫外線照射眼與對(duì)側(cè)未照射眼的晶狀體內(nèi)GPx活性的差值,與紫外線照射后第3天和第7天比較,差異有統(tǒng)計(jì)學(xué)意義。紫外線照射后1-7天晶狀體內(nèi)GSSG濃度和GR活性均無顯著性變化。 結(jié)論：近閾值量紫外線照射(UVR-300 nm)可以改變大鼠晶狀體內(nèi)谷胱甘肽氧化還原平衡狀態(tài),并啟動(dòng)晶狀體細(xì)胞內(nèi)適應(yīng)性抗氧化反應(yīng)；晶狀體混濁度隨紫外線照射后時(shí)間增加逐漸加重；近閾值量紫外線照射后1周晶狀體形態(tài)學(xué)和細(xì)胞內(nèi)氧化還原體系均未恢復(fù)到正常狀態(tài)。 實(shí)驗(yàn)二： α-生育酚對(duì)紫外線誘導(dǎo)的大鼠白內(nèi)障保護(hù)作用量效關(guān)系的實(shí)驗(yàn)研究 目的：探討α-生育酚對(duì)紫外線誘導(dǎo)的大鼠白內(nèi)障的保護(hù)作用與口服α-生育酚劑量之間的量效關(guān)系；闡述α-生育酚對(duì)紫外線照射后晶狀體內(nèi)谷胱甘肽氧化還原體系的影響及晶狀體內(nèi)不同抗氧化劑之間的相互作用。 方法：100只6周齡的albino Spraque Dawley雌性大鼠隨機(jī)分為5組,每組20只。4個(gè)實(shí)驗(yàn)組大鼠每日給予α-生育酚喂養(yǎng),劑量分別為5、25、50和100 IU/天；另一組無α-生育酚喂養(yǎng)的大鼠為對(duì)照組。喂養(yǎng)4周后,所有大鼠單側(cè)眼行紫外線照射(UVR-300 nm,8 kJ/m2)15分鐘。大鼠分別于紫外線照射后1周處死,摘除雙側(cè)眼球,分離晶狀體,測(cè)量晶狀體光散射強(qiáng)度,定量分析晶狀體混濁度,暗背景光晶狀體照像,分光光度法測(cè)定晶狀體內(nèi)GSH/GSSG濃度及GR/GPx的活性。紫外線照射眼晶狀體與對(duì)側(cè)未照射眼晶狀體各項(xiàng)實(shí)驗(yàn)參數(shù)差值的平均值作為統(tǒng)計(jì)學(xué)分析的原始數(shù)據(jù)。 結(jié)果：α-生育酚喂養(yǎng)組大鼠紫外線照射眼僅出現(xiàn)表淺和輕度的晶狀體混濁；對(duì)照組大鼠紫外線照射眼則出現(xiàn)明顯的皮質(zhì)性和致密的赤道部晶狀體混濁。所有大鼠紫外線照射眼的晶狀體光散射強(qiáng)度均高于對(duì)側(cè)未照射眼：紫外線照射眼與對(duì)側(cè)未照射眼晶狀體光散射強(qiáng)度的差值,隨口服α-生育酚劑量增加而逐漸下降(速率常數(shù)為4.5),當(dāng)α-生育酚劑量超過25 IU/天以上后,晶狀體光散射強(qiáng)度的變化趨于平穩(wěn)；各實(shí)驗(yàn)組大鼠與對(duì)照組大鼠晶狀體光散射強(qiáng)度差值比較,差異均有統(tǒng)計(jì)學(xué)意義。紫外線照射后大鼠晶狀體內(nèi)GSH濃度明顯下降；GSH的下降量隨口服α-生育酚劑量的增加而逐漸減小(速率常數(shù)為52),當(dāng)α-生育酚劑量超過25 IU/天以上后,晶狀體內(nèi)GSH的下降量漸趨平穩(wěn)；對(duì)照組和小劑量(5IU/天)α-生育酚喂養(yǎng)組大鼠,與大劑量(25-100 IU/天)α-生育酚喂養(yǎng)組大鼠比較,紫外線照射后晶狀體內(nèi)GSH的下降量,差異有統(tǒng)計(jì)學(xué)意義。α-生育酚喂養(yǎng)組大鼠與對(duì)照組大鼠紫外線照射后晶狀體內(nèi)GSSG濃度及GR/GPx活性均無顯著性變化。 結(jié)論：α-生育酚對(duì)紫外線誘導(dǎo)的大鼠白內(nèi)障的保護(hù)作用與口服α-生育酚的劑量呈劑量依賴關(guān)系。α-生育酚能夠降低紫外線照射后晶狀體的混濁程度,但不能完全阻止白內(nèi)障的發(fā)生。α-生育酚能夠減少紫外線照射后晶狀體內(nèi)GSH的消耗,其保護(hù)作用與口服α-生育酚的劑量呈劑量依賴關(guān)系。紫外線照射導(dǎo)致的大鼠白內(nèi)障只有在晶狀體內(nèi)GSH的下降量超出其閾值時(shí)才會(huì)發(fā)生。口服α-生育酚不能改變紫外線照射后晶狀體內(nèi)GSSG的濃度及GR/GPx的活性。
[Abstract]:Clinical significance
Cataract is the first blind eye disease in the world, and the oxidative damage of the lens is the main mechanism of cataract formation. A large number of clinical and epidemiological studies have confirmed that ultraviolet radiation (UVR) is one of the most important risk factors for the formation and development of human cataracts. It also increases the radiation of ultraviolet radiation to the earth, inevitably endangers human health and greatly increases the dangers of cataract formation. At the same time, the incidence of cataracts will continue to rise as the world population grows and population aging, and the public health problems and economic burdens caused by cataracts are increasing. It is important for us to study the mechanism of cataract formation and development by ultraviolet radiation, to explore the new requirements for the protection of the antioxidation defense system in the crystalline body, and to put forward higher targets for the new methods for the study and development of non operative prevention and delayed cataract. Therefore, WHO proposes to protect ultraviolet radiation and study it. Low cost antioxidants are the primary goal of preventing and delaying cataract.
The purpose of this study is to establish a rat model of cataract induced by near threshold ultraviolet (UVR-300nm). Using the method of measuring the intensity of light scattering of the lens, the degree of turbidity in the lens after ultraviolet radiation is quantitatively studied and dynamic observed. The quantitative analysis and dynamic study of the corresponding biochemical indexes in the peptide redox system were carried out to further explore the mechanism of ultraviolet induced cataract formation and development. At the same time, the quantitative relationship between the protective effect of alpha tocopherol (vitamin E) on ultraviolet induced cataract in rats and its dose, and the alpha birth were studied and discussed. The effect and interaction of phenol on the glutathione redox system in the crystalline body after ultraviolet irradiation, provide detailed experimental data for the future research on alpha tocopherol protection against ultraviolet radiation cataract, and better develop and utilize the important biological functions of vitamin E, for the clinical application of vitamin E to prevent and delay cataract The development provides the basis for the experiment.
Experiment 1:
Changes of glutathione redox balance in rat cataract induced by ultraviolet light
Objective: To observe the changes of rat cataracts induced by near threshold ultraviolet (UVB) and to study the dynamic changes in the system of GSH redox balance at different times after ultraviolet radiation, and to explore the mechanism of ultraviolet induced cataract formation and development.
Methods: 40 6 weeks old albino Spraque Dawley female rats were randomly divided into 4 groups, with 10 rats in each group. The experimental group was irradiated with ultraviolet radiation (UVR-300 nm, 8 kJ/m2) for 15 minutes. The other group of rats without ultraviolet radiation was killed in 1,3 and 7 days after ultraviolet radiation in the normal control group, and the two groups were removed. Side eyeball, lens separation, measurement of light scattering intensity of lens, quantitative analysis of lens turbidity, dark background photo lens, spectrophotometric determination of reduced glutathione, GSH and oxidized glutathione, GSSG Valley caspin concentration and glutathione reductase (glutathione reductase, GR) and valley The activity of glutathione peroxidase (GPx) in the normal control group, provided the baseline values of the experimental parameters of the normal lens of the rat. The mean value of the difference between the lens of the ultraviolet light and the experimental parameters of the unirradiated eye lens was used as the original data of the analysis.
Results: the degree of lens opacity increased gradually with the increase of the time after ultraviolet radiation, while there was no obvious turbidity in the lens of the normal control group and the lens of the experimental group, and the difference between the ultraviolet light and the light scattering intensity of the unirradiated eye was normal. The difference was statistically significant in the lens of the rats. The concentration of GSH in the crystalline body increased at first days after ultraviolet radiation, and then the concentration of GSH decreased gradually with the increase of the time after irradiation, and the concentration of GSH was still not recovered to the normal level at seventh days after ultraviolet radiation, and the ultraviolet rays irradiated the eye first days after ultraviolet radiation. The difference in the concentration of GSH in the unirradiated eyes was statistically significant compared with the third and seventh days after ultraviolet irradiation. The activity of GPx in the crystalline body appeared to be enhanced at first days after ultraviolet radiation, and then the activity of GPx decreased gradually with the increase of the irradiation time, and the activity of GPx was restored to normal after the ultraviolet radiation. The difference of GPx activity between ultraviolet light and unirradiated eye first days after ultraviolet radiation was statistically significant compared with the third days and seventh days after ultraviolet radiation. There was no significant change in the concentration of GSSG and the activity of GR in the crystalline body 1-7 days after ultraviolet irradiation.
Conclusion: near threshold ultraviolet radiation (UVR-300 nm) can change the redox equilibrium state of glutathione in the rat crystalline body and initiate the adaptive antioxidant reaction in the lens cells, and the lens opacity increases gradually with the increase of the time after ultraviolet radiation, and the morphology and cell of the lens are 1 weeks after the near threshold ultraviolet radiation. The redox system did not recover to the normal state.
Experiment two:
Experimental study on dose effect relationship of alpha tocopherol on ultraviolet induced cataract in rats
Objective: To investigate the relationship between the protective effect of alpha tocopherol on ultraviolet induced cataract in rats and the dose effect of oral alpha tocopherol, and the effect of alpha tocopherol on the redox system of glutathione in crystalline body after ultraviolet irradiation and the interaction between different antioxidants in the crystalline body.
Methods: 100 6 weeks old albino Spraque Dawley female rats were randomly divided into 5 groups. Each group of 20 rats in each group was given alpha tocopherol every day with a dose of 5,25,50 and 100 IU/ days, and the other group without alpha tocopherol was fed as the control group. After feeding for 4 weeks, the unilateral eyes of all rats were irradiated with ultraviolet radiation (UVR-300 nm, 8 kJ/m2). ) 15 minutes. The rats were killed at 1 weeks after the ultraviolet radiation, the lens was removed, the lens was separated, the light scattering intensity of the lens was measured, the lens opacity, the dark background light lens were quantified, the concentration of GSH/GSSG in the crystalline body and the viability of the GR/GPx were measured by spectrophotometry. The lens of the ultraviolet light and the unirradiated eye in the opposite side The average value of the experimental parameters difference is the original data of statistical analysis.
Results: only light and mild lens opacities were found in the ultraviolet light of the rats in the alpha tocopherol feeding group, and the ultraviolet light in the control group showed obvious cortical and dense equatorial lens opacities. The intensity of the light scattering of the ultraviolet light in all rats was higher than that in the unirradiated eye: ultraviolet radiation. The difference between the light scattering intensity of the eye and the contralateral unirradiated eyes gradually decreased with the increase of the dose of alpha tocopherol (rate constant 4.5). When the dose of alpha tocopherol exceeded 25 IU/ days, the change of light scattering intensity of the lens tended to be stable; the difference between the experimental group and the lens light scattering intensity difference between the experimental group and the rats was poor. The concentration of GSH decreased significantly in the crystalline body of rats after ultraviolet radiation, and the decrease of GSH gradually decreased with the increase of oral alpha tocopherol dose (rate constant was 52). When alpha tocopherol dose exceeded 25 IU/ days, the decrease of GSH in the crystalline body gradually became stable; the control group and small dose (5IU/ days) alpha birth Compared with the large dose (25-100 IU/ days) alpha tocopherol feeding rats, the decrease of GSH in the crystalline body after ultraviolet irradiation was statistically significant. There was no significant change in the concentration of GSSG and the activity of GR/GPx in the crystalline body of the rats of the alpha tocopherol feeding group and the control group.
Conclusion: the protective effect of alpha tocopherol on ultraviolet induced cataract in rats is dependent on the dose of oral alpha tocopherol. Alpha tocopherol can reduce the turbidity of the lens after ultraviolet radiation, but can not completely prevent the occurrence of cataract. Alpha tocopherol can reduce the consumption of GSH in the crystalline body after ultraviolet radiation. The protective effect is in a dose-dependent manner with the dose of oral alpha tocopherol. The cataract induced by ultraviolet radiation occurs only when the decrease of GSH in the crystalline body exceeds its threshold. The oral alpha tocopherol can not change the concentration of GSSG in the crystalline body and the activity of GR/GPx in the crystalline body after ultraviolet radiation.
【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2010
【分類號(hào)】：R776.1

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