本文選題：青光眼 + 神經(jīng)退行性病變　； 參考：《華中科技大學(xué)》2013年博士論文

【摘要】：青光眼是一種復(fù)雜的致盲性神經(jīng)退行性疾病。青光眼的神經(jīng)退行性病變發(fā)生在視網(wǎng)膜神經(jīng)節(jié)細(xì)胞及視神經(jīng)軸突,涉及先天遺傳傾向,后天危險因素以及與年齡增長相關(guān)的環(huán)境刺激。眼內(nèi)壓升高被認(rèn)為是青光眼疾病發(fā)生發(fā)展的重要危險因素之一,也是目前可以干預(yù)的因素。至今青光眼的治療還是基于降低眼壓。近年來研究發(fā)現(xiàn),除了眼壓升高,在青光眼中多種刺激因素影響了細(xì)胞內(nèi)環(huán)境穩(wěn)定,而且神經(jīng)元對刺激因素的抵抗力也決定了其內(nèi)在易感性。有證據(jù)顯示當(dāng)視網(wǎng)膜神經(jīng)節(jié)細(xì)胞暴露在青光眼性壓力刺激下,導(dǎo)致其出現(xiàn)一系列相關(guān)聯(lián)的細(xì)胞下游通路活動,包括線粒體功能異常,蛋白水解級聯(lián)反應(yīng),內(nèi)質(zhì)網(wǎng)壓力和氧化應(yīng)激等。引起神經(jīng)起始損傷和青光眼性神經(jīng)退行性病變的具體分子機(jī)制一直在被廣泛研究并存在很大爭議。 青光眼神經(jīng)節(jié)細(xì)胞損傷的因素有很多,目前有很多學(xué)說試圖解釋青光眼的發(fā)病機(jī)制,如機(jī)械壓力學(xué)說、氧化應(yīng)激學(xué)說等,而最近研究的熱點(diǎn)是青光眼的自身免疫和異常蛋白沉淀這兩大方面：研究發(fā)現(xiàn)青光眼神經(jīng)退行性病變涉及免疫系統(tǒng),包括天然免疫和獲得免疫在內(nèi)的不同成分,還有越來越多的證據(jù)將青光眼的發(fā)病機(jī)制指向補(bǔ)體系統(tǒng)的激活,補(bǔ)體激活的產(chǎn)物,如Clq, C3和膜攻擊復(fù)合物(MAC)在青光眼模型動物和青光眼病人的視網(wǎng)膜中被發(fā)現(xiàn)。本研究的前兩個部分試圖探討補(bǔ)體系統(tǒng)的激活在青光眼發(fā)病機(jī)制中所扮演的角色。第一部分為體內(nèi)研究,連續(xù)觀察補(bǔ)體系統(tǒng)相關(guān)蛋白在大鼠青光眼模型中的變化。第二部分為體外研究,探討補(bǔ)體系統(tǒng)激活終產(chǎn)物膜攻擊復(fù)合物C5b-9對視網(wǎng)膜神經(jīng)節(jié)細(xì)胞凋亡和程序化壞死的影響。另一方面,神經(jīng)退行性病變是指神經(jīng)元細(xì)胞在結(jié)構(gòu)及功能上的逐漸損失,最終死亡的病變,其發(fā)病機(jī)理涉及蛋白的異常加工,錯誤折疊以及在蛋白在細(xì)胞內(nèi)外的異常聚集。視網(wǎng)膜也是中樞神經(jīng)系統(tǒng)的一部分,因此在神經(jīng)退行性病變的進(jìn)程中,視網(wǎng)膜和視神經(jīng)會受到相似的影響。異常蛋白在神經(jīng)元的沉積,包括Ap和異常Tau蛋白的沉積,是神經(jīng)節(jié)細(xì)胞另一損傷因素。本研究第三部分是觀察Tau蛋白在青光眼視網(wǎng)膜中的變化并探討氯化鋰在慢性青光眼神經(jīng)退行性病變的作用及治療機(jī)制。 第一部分：大鼠青光眼模型中補(bǔ)體系統(tǒng)相關(guān)蛋白的變化 目的：研究補(bǔ)體系統(tǒng)的激活對慢性青光眼高眼壓模型中視網(wǎng)膜神經(jīng)節(jié)細(xì)胞的影響。 方法：用DA大鼠構(gòu)建慢性高眼壓模型,將動物分成4組,每組5只,左眼為手術(shù)眼,通過往鞏膜靜脈注射高滲鹽水的方法提高眼內(nèi)壓,右眼不做處理作為正常對照眼。動物自手術(shù)后1周,3周,8周和16周分別處死,免疫熒光法測試高眼壓眼和對照眼視網(wǎng)膜內(nèi)的膜攻擊復(fù)合物(MAC, C5b-9), C3和衰變加速因子(DAF)的表達(dá)水平。 結(jié)果：C5b-9自青光眼大鼠眼壓升高8周起表達(dá)明顯上調(diào),C3的表達(dá)在高眼壓中也有所提高。而衰變加速因子DAF的表達(dá)發(fā)現(xiàn)在8周和16周高眼壓組明顯降低。 結(jié)論：在慢性青光眼動物模型視網(wǎng)膜節(jié)細(xì)胞層補(bǔ)體活動產(chǎn)物上調(diào)和補(bǔ)體調(diào)節(jié)蛋白衰變加速因子DAF的下降提示補(bǔ)體激活和補(bǔ)體調(diào)節(jié)的失衡,此現(xiàn)象是否在青光眼的發(fā)病機(jī)制中扮演潛在作用還需進(jìn)一步研究。 第二部分：膜攻擊復(fù)合物C5b-9對視網(wǎng)膜神經(jīng)節(jié)細(xì)胞的凋亡和程序化壞死的影響 目的：視網(wǎng)膜神經(jīng)節(jié)細(xì)胞的損失是青光眼的特征,但是神經(jīng)節(jié)細(xì)胞死亡的調(diào)節(jié)機(jī)制仍未研究清楚。本部分的研究目的是確定膜攻擊復(fù)合物C5b-9是否誘導(dǎo)神經(jīng)節(jié)細(xì)胞的死亡和／或者調(diào)節(jié)了視網(wǎng)膜神經(jīng)節(jié)細(xì)胞對其他細(xì)胞壓力作用的敏感性。 方法：本研究使用RGC-5細(xì)胞系為研究對象,用抗CD59抗體阻斷CD59后, RGC-5細(xì)胞作用于正常人血清,用免疫熒光染色法觀察細(xì)胞形態(tài)學(xué),流式細(xì)胞技術(shù)以及用PARP剪切和活化的caspase-3作為探針的western blot技術(shù)檢測細(xì)胞凋亡的程度。同時用程序化壞死抑制劑AGK2作用于細(xì)胞,用流式細(xì)胞技術(shù)檢測細(xì)胞程序性壞死的程度。在有或沒C5b-9生成的條件下,ionomycin, staurosporine,雙氧化氫和chelerythrine對RGC-5細(xì)胞的敏感性的變化也被觀察。 結(jié)果：在暴露于C5b-9的條件下,RGC-5細(xì)胞出現(xiàn)凋亡。RGC-5細(xì)胞還在staurosporine作用后出現(xiàn)凋亡,但對ionomycin和過氧化氫存在抵抗作用。C5b-9能夠明顯增加staurosporine引發(fā)RGC-5細(xì)胞凋亡和程序化壞死的敏感度。 結(jié)論：低水平的C5b-9可以引起RGC-5細(xì)胞的凋亡,應(yīng)用不同的激動劑證實(shí)C5b-9能特異地敏感化一些凋亡和程序化壞死的通路。研究結(jié)果揭示了補(bǔ)體系統(tǒng)在視網(wǎng)膜神經(jīng)節(jié)細(xì)胞損失中的潛在作用。 第三部分：Tau蛋白在鼠慢性青光眼模型中的變化和機(jī)制研究 目的：研究在慢性青光眼性損害時視網(wǎng)膜神經(jīng)節(jié)細(xì)胞層中Tau蛋白磷酸化的變化,并通過利用氯化鋰抑制Tau上游激酶GSK-3β活性的實(shí)驗(yàn),為在臨床上用氯化鋰治療慢性青光眼神經(jīng)退行性病變提供實(shí)驗(yàn)依據(jù)。 方法：建立慢性高眼壓SD大鼠模型,分為兩組各10只。一組為高眼壓未治療組,右眼為高眼壓模型眼,左眼為正常對照眼；另一組為高眼壓氯化鋰治療組,治療組于建模當(dāng)天起每日腹腔注射0.6M氯化鋰(GSK-3β抑制劑)。在第2周和第4周從兩組中各取5只大鼠處死并摘取眼球,用免疫熒光和Western blot觀察視網(wǎng)膜總Tau和磷酸化Tau蛋白的變化。 結(jié)果：1)高眼壓模型視網(wǎng)膜Tau蛋白及其磷酸化水平發(fā)生了改變：總Tau含量在第2周時下降為對照眼的77.3%,在第4周時下降為對照組的60.4%; p-Tau與總Tau的比值,在第2周時幾乎沒有變化,在第4周時增加到對照眼的135.4%,磷酸化明顯增加。2)氯化鋰對高眼壓模型鼠的影響：在第4周時,氯化鋰治療組視網(wǎng)膜總Tau含量較未治療組明顯升高,為對照眼的99%;p-Tau與總Tau的比值較未治療組明顯下降,幾乎降到對照眼水平。結(jié)論：持續(xù)高眼壓刺激導(dǎo)致大鼠視網(wǎng)膜總Tau蛋白表達(dá)量降低,Tau蛋白磷酸化水平增加；氯化鋰能減輕由持續(xù)高眼壓引起的Tau蛋白的過度磷酸化,其機(jī)制還需進(jìn)一步研究。 研究總結(jié) 一、主要研究結(jié)果 1.在慢性高眼壓模型鼠中,膜攻擊復(fù)合物C5b-9在視網(wǎng)膜神經(jīng)節(jié)細(xì)胞層的表達(dá)在眼壓升高第8周明顯上升,補(bǔ)體激活途徑樞紐蛋白C3在慢性高眼壓模型中的表達(dá)也上調(diào)。補(bǔ)體調(diào)節(jié)蛋白衰變加速因子(DAF)的表達(dá)在高眼壓第8周明顯下降,與C5b-9的表達(dá)變化相對應(yīng)。 2.體外研究發(fā)現(xiàn)膜攻擊復(fù)合物C5b-9可在RGC-5細(xì)胞上被誘導(dǎo)生成。C5b-9的生成可誘導(dǎo)RGC-5細(xì)胞的發(fā)生凋亡。C5b-9能夠明顯增加staurosporine引發(fā)細(xì)胞凋亡和程序化壞死的敏感度。 3.在慢性高眼壓模型鼠中,總Tau含量在高眼壓第2周時已下降,在第4周進(jìn)一步降低,在第4周Tau蛋白的磷酸化明顯增加；氯化鋰治療組在第4周時視網(wǎng)膜總Tau含量較未治療組明顯升高,磷酸化程度較未治療組明顯下降。 二、研究結(jié)論 1.在慢性青光眼動物模型中,視網(wǎng)膜節(jié)細(xì)胞層各補(bǔ)體活動產(chǎn)物上調(diào)和補(bǔ)體條件蛋白DAF的下降提示補(bǔ)體激活和補(bǔ)體調(diào)節(jié)的失衡可能在青光眼的發(fā)病機(jī)制中扮演潛在作用。 2.低水平的C5b-9可以引起RGC-5細(xì)胞的凋亡,并通過多種不同的激動劑的運(yùn)用,進(jìn)一步證實(shí)了C5b-9能特異地使細(xì)胞的一些凋亡和程序化壞死的通路敏感化。 3.在慢性青光眼動物模型中,持續(xù)高眼壓刺激導(dǎo)致大鼠視網(wǎng)膜總Tau蛋白表達(dá)量降低,Tau蛋白磷酸化水平增加；氯化鋰能減輕由持續(xù)高眼壓引起的Tau蛋白的過度磷酸化。
[Abstract]:Glaucoma is a complex, blinding neurodegenerative disease. Neurodegenerative diseases of glaucoma occur in retinal ganglion cells and optic axons, involving congenital genetic tendencies, acquired risk factors and environmental stimuli associated with age growth. Elevated intraocular pressure is recognized as an important risk for the development of glaucoma. One factor, it is also a factor that can be used to intervene now. The treatment of glaucoma is still based on the reduction of intraocular pressure. In recent years, it has been found that in addition to increased intraocular pressure, a variety of stimuli in glaucoma affect the stability of the intracellular environment, and the resistance of neurons to stimulating factors also determines its intrinsic susceptibility. Membrane ganglion cells are exposed to glaucoma pressure stimulation, resulting in a series of associated downstream pathway activities, including mitochondrial dysfunction, proteolysis cascade, endoplasmic reticulum pressure and oxidative stress. The specific molecular mechanisms that cause nerve initial damage and glaucomatous degenerative diseases have been widely used. There is a lot of controversy in the pan study.
There are many factors for the injury of ganglion cells in glaucoma. There are many theories to explain the pathogenesis of glaucoma, such as the theory of mechanical stress, the theory of oxidative stress and so on. The recent research focuses on the two major aspects of the autoimmune and abnormal protein precipitation of glaucoma. The study found that the neurodegenerative diseases of glaucoma involve the immune system. There is a growing number of evidence to point the pathogenesis of glaucoma to the activation of the complement system. The products activated by complement, such as Clq, C3 and membrane attack complex (MAC), are found in the retina of glaucoma model animals and glaucoma patients. The first two parts of this study attempt To explore the role of complement system activation in the pathogenesis of glaucoma. The first part is in vivo study to observe the changes of complement system related proteins in the rat model of glaucoma. The second part is in vitro study to explore the apoptosis and process of retinal ganglion cells by the complement system activation terminal product membrane attack complex C5b-9. On the other hand, neurodegenerative disease refers to the gradual loss of neuronal cells in structure and function, the eventual death of the lesion, and its pathogenesis involves abnormal processing of proteins, misfolding and abnormal aggregation of proteins in and out of cells. The retina is part of the central nervous system and therefore is in the nerve. In the process of degenerative disease, the retina and optic nerve are affected by similar effects. Abnormal protein deposition in neurons, including the deposition of Ap and abnormal Tau protein, is another damage factor of the ganglion cells. The third part of this study was to observe the changes in the Tau protein in the glaucoma retina and to explore the retrogression of lithium chloride in the chronic glaucoma. The role and therapeutic mechanism of progressive lesions.
Part one: changes of complement system related proteins in rat glaucoma models
Objective: To study the effect of complement system activation on retinal ganglion cells in chronic glaucoma with high intraocular pressure.
Methods: the model of chronic ocular hypertension was constructed in DA rats. The animals were divided into 4 groups, 5 in each group, and the left eye was the operation eye. The intraocular pressure was improved by injection of hypertonic saline into the scleral vein. The right eye was not treated as the normal eye. The animals were killed at 1, 3, 8 and 16 weeks after the operation. High intraocular pressure and control were tested by immunofluorescence. The retinal inner membrane attacks the expression levels of MAC (C5b-9), C3 and decay accelerating factor (DAF).
Results: the expression of C5b-9 was up obviously up to 8 weeks from the increase of intraocular pressure in glaucoma rats, and the expression of C3 increased in high intraocular pressure. The expression of the decay accelerating factor DAF was obviously decreased in the high intraocular pressure group at 8 and 16 weeks.
Conclusion: the up-regulation of complement activity products and the decline of complement regulatory protein decay acceleration factor DAF in the retinal ganglion cell layer of chronic glaucoma animal models suggest the imbalance of complement activation and complement regulation. It is still necessary to study the potential role of this phenomenon in the pathogenesis of glaucoma.
The second part: effect of membrane attack complex C5b-9 on apoptosis and programmed necrosis of retinal ganglion cells.
Objective: the loss of retinal ganglion cells is a characteristic of glaucoma, but the mechanism of the regulation of ganglion cell death is still not clear. The purpose of this part is to determine whether the membrane attack complex C5b-9 induces the death of ganglion cells and / or regulates the sensitivity of the retinal ganglion cells to the pressure of other cells. Sex.
Methods: in this study, the RGC-5 cell line was used as the research object. After blocking the CD59 with anti CD59 antibody, the RGC-5 cells acted on the normal human serum. The cell morphology was observed by immunofluorescence staining, the flow cytometry and the Western blot technology with PARP and activated caspase-3 as the probe were used to detect the degree of apoptosis. Sequence necrosis inhibitor AGK2 acts on cells, and the degree of programmed cell necrosis is detected by flow cytometry. The changes in sensitivity of ionomycin, staurosporine, hydrogen peroxide and chelerythrine to RGC-5 cells are also observed under or without C5b-9 formation.
Results: under the condition of exposure to C5b-9, apoptotic.RGC-5 cells in RGC-5 cells were also apoptotic after the action of staurosporine, but the resistance to ionomycin and hydrogen peroxide could significantly increase the sensitivity of staurosporine to apoptosis and programmed necrosis of RGC-5 cells.
Conclusion: low level of C5b-9 can induce apoptosis of RGC-5 cells. Different agonists have been used to confirm that C5b-9 can sensitize some apoptotic and programmed necrosis pathways specifically. The results reveal the potential role of complement system in retinal ganglion cell loss.
The third part: the change and mechanism of Tau protein in rat chronic glaucoma model.
Objective: To study the changes in the phosphorylation of Tau protein in the retinal ganglion cell layer of chronic glaucomatous damage, and to provide evidence for the clinical use of lithium chloride in the treatment of neurodegenerative diseases of chronic glaucoma by using lithium chloride to inhibit the activity of Tau upstream kinase GSK-3 beta.
Methods: the chronic high intraocular pressure SD rat model was established and divided into two groups of 10 rats. One group was the untreated group with high intraocular pressure, the right eye was the high intraocular pressure model eye, the left eye was normal to the eye, the other group was the high intraocular pressure lithium chloride treatment group. The treatment group Yu Jianmo was intraperitoneally injected with 0.6M lithium chloride (GSK-3 beta inhibitor) daily from the day of second and fourth weeks from two groups. 5 rats in each group were sacrificed and their eyeballs were removed. The changes of total Tau and phosphorylation of Tau protein were observed by immunofluorescence and Western blot.
Results: 1) the retinal Tau protein and its phosphorylation level in the high intraocular pressure model were changed: the total Tau content decreased to 77.3% in the control eye at second weeks and 60.4% in the control group at fourth weeks; the ratio of p-Tau to the total Tau was almost unchanged at second weeks, and increased to 135.4% of the control eye at fourth weeks, and phosphorylation significantly increased.2. The effect of lithium chloride on the high intraocular pressure model rats: at fourth weeks, the total retinal Tau content in the lithium chloride treatment group was significantly higher than that in the untreated group, which was 99% of the control eye. The ratio of p-Tau to the total Tau decreased significantly than that in the untreated group, almost to the control eye level. Conclusion: the sustained high intraocular pressure induced the decrease of the total Tau protein expression in the retina of rats. The level of Tau protein phosphorylation is increased. Lithium chloride can alleviate the excessive phosphorylation of Tau protein induced by sustained high intraocular pressure, and its mechanism needs further study.
Research Summary
First, the main research results
1. in the chronic high intraocular pressure model rats, the expression of membrane attack complex C5b-9 in the retinal ganglion cell layer increased obviously for eighth weeks, and the expression of the complement activation pathway hub protein C3 in the chronic high intraocular pressure model was also up-regulated. The expression of complement regulatory protein decay acceleration factor (DAF) decreased significantly at the high intraocular pressure for eighth weeks, and C5b-9 The change of expression is corresponding.
2. in vitro study found that membrane attack complex C5b-9 can be induced to produce.C5b-9 on RGC-5 cells and induce apoptosis of RGC-5 cells to induce apoptosis.C5b-9, which can significantly increase the sensitivity of staurosporine to cell apoptosis and programmed necrosis.
3. in the chronic high intraocular pressure model rats, the total Tau content decreased at the second week of high intraocular pressure, decreased further in the fourth week, and the phosphorylation of Tau protein increased significantly at fourth weeks, and the total Tau content in the retina group was significantly higher than that in the untreated group at fourth weeks, and the degree of phosphorylation was significantly lower than that in the untreated group.
Two, the conclusion of the study
1. in the animal model of chronic glaucoma, the up regulation of complement activity products and the decrease of complement conditional protein DAF in the retinal ganglion cell layer suggest that the imbalance of complement activation and complement regulation may play a potential role in the pathogenesis of glaucoma.
2. the low level of C5b-9 can induce apoptosis of RGC-5 cells and, through the use of a variety of different agonists, further confirmed that C5b-9 can sensitize some of the cell apoptosis and programmed necrosis in a special way.
3. in the animal model of chronic glaucoma, persistent high intraocular pressure (IOP) stimulates the decrease of the total Tau protein expression in the retina and the increased phosphorylation of Tau protein, and lithium chloride can reduce the excessive phosphorylation of Tau protein caused by persistent high intraocular pressure.
【學(xué)位授予單位】：華中科技大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2013
【分類號】：R775

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