本文選題：慢性高眼壓模型 + RGCRGCs　； 參考：《山西醫(yī)科大學(xué)》2011年碩士論文

【摘要】：目的：在構(gòu)建小鼠慢性高眼壓模型的基礎(chǔ)上，觀察白血病抑制因子(Leukemiainhibitory factor, LIF)對(duì)生長(zhǎng)相關(guān)蛋白-43 (growth associated protein-43，GAP-43)在小鼠眼視網(wǎng)膜神經(jīng)節(jié)細(xì)胞（retinal ganglion cells，RGCs）及其他部位中的表達(dá)影響，探討其對(duì)小鼠慢性高眼壓模型中視網(wǎng)膜神經(jīng)節(jié)細(xì)胞的保護(hù)作用，為臨床治療RGCs呈慢性喪失且病因不清的疾�。ㄈ缜喙庋�、視網(wǎng)膜色素變性等）提供一種有效的輔助方法。 方法：將60只正常無(wú)眼疾昆明小鼠(60只眼)隨機(jī)分為正常對(duì)照組（20只小鼠，20只眼）慢性高眼壓組(20只小鼠，20只眼)、LIF治療組（20只小鼠，20只眼）。每組根據(jù)治療后觀察時(shí)間分為用藥前，用藥后1天、7天、14天4個(gè)小組（每小組5只小鼠，5只眼）。采用燒灼小鼠鞏膜表層的房水引流靜脈建立小鼠慢性高眼壓模型，于模型成功后（眼壓穩(wěn)定升高1周后）向小鼠玻璃體腔內(nèi)注射0.5ul/g LIF。分別于用藥前，用藥后1天、7天、14天摘除眼球，，固定、石蠟包埋、切片，進(jìn)行HE染色及免疫組織化學(xué)染色。普通光學(xué)顯微鏡下觀察視網(wǎng)膜形態(tài)變化，應(yīng)用醫(yī)學(xué)圖像分析系統(tǒng)對(duì)進(jìn)行RGCs量化及GAP-43表達(dá)的灰度分析，進(jìn)行統(tǒng)計(jì)學(xué)處理。 結(jié)果： 1.眼壓變化：治療組與慢性高眼壓組在用藥前及用藥后即刻觀察小鼠眼壓相較差異無(wú)顯著性（P0.05）而相較于正常對(duì)照組增高，治療組在隨后1天、7天、14天比慢性高眼壓組眼壓降低，但并不明顯，較正常對(duì)照組眼壓仍高，差異有顯著性（P0.05）。 2.組織形態(tài)觀察：慢性高眼壓組織學(xué)變化早期為視網(wǎng)膜神經(jīng)纖維層、內(nèi)叢狀層水腫。晚期視網(wǎng)膜內(nèi)層水腫消退，萎縮、變薄，視網(wǎng)膜神經(jīng)節(jié)細(xì)胞數(shù)目減少。治療組相較于慢性高眼壓組水腫消退較快，萎縮不明顯，視網(wǎng)膜神經(jīng)節(jié)細(xì)胞數(shù)目減少不明顯。 3.RGCs計(jì)數(shù)結(jié)果：治療組與慢性高眼壓組在治療前及治療后1天觀察RGCs數(shù)目相比較差異無(wú)顯著性（P0.05）而相較于正常對(duì)照組數(shù)目減少，慢性高眼壓組在隨后7天、14天比治療組RGCs數(shù)目減少明顯，差異有顯著性（P0.05）。但治療組較正常對(duì)照組數(shù)目仍少，差異有顯著性（P0.05）。 4.免疫組織化學(xué)觀察：GAP-43表達(dá)于各組視網(wǎng)膜神經(jīng)纖維層、RGCs、以及內(nèi)叢狀層上。通過(guò)灰度分析比較，慢性高眼壓組早期可見(jiàn)GAP-43的表達(dá)增加，隨后表達(dá)逐漸減少，晚期接近正常；而治療組早期即可見(jiàn)GAP-43的表達(dá)增加，且在觀察期內(nèi)穩(wěn)定增加，且各期間相較差異有顯著性（P0.05）。 結(jié)論： 1.病理學(xué)及眼壓改變顯示小鼠慢性高眼壓模型建模成功。 2.LIF在小鼠慢性高眼壓模型中促進(jìn)GAP-43的表達(dá)增加。 3.LIF對(duì)小鼠慢性高眼壓模型中視網(wǎng)膜神經(jīng)節(jié)細(xì)胞具有保護(hù)作用。
[Abstract]:Objective: to investigate the effect of Leukemiae inhibitor factor (LIF-43 associated protein-43) on the expression of associated protein 43 in the retinal ganglion cells (RGCs) and other parts of the retinal ganglion cells in mice, and to investigate the effect of Leukemiae inhibitor factor (LIF-43) on the expression of RGCsin the retinal ganglion cells. To investigate its protective effect on retinal ganglion cells (RGCs) in mice with chronic intraocular hypertension, and to provide an effective method for the treatment of RGCs with chronic loss and unclear etiology (such as glaucoma, retinitis pigmentosa, etc.). Methods: sixty eyes of Kunming mice were randomly divided into control group (n = 20, n = 20) and chronic intraocular hypertension group (n = 20, n = 20). Each group was divided into 4 groups according to the time of observation after treatment and 4 groups (5 mice in each group) and 4 groups (5 eyes in each group). A chronic intraocular pressure model was established by cauterizing the aqueous humor drainage veins in the scleral surface of mice. 0.5ul/g lif was injected into the vitreous cavity of mice after the success of the model (1 week after the stable elevation of intraocular pressure). The eyeballs were removed, fixed, embedded in paraffin wax, sectioned, stained with HE and immunohistochemical staining before and 1 day after treatment. The morphological changes of retina were observed under general optical microscope. The quantitative analysis of RGCs and the gray level of GAP-43 expression were analyzed by medical image analysis system. Results: 1. IOP changes: there was no significant difference in intraocular pressure between the treatment group and the chronic high intraocular pressure group before and immediately after treatment (P 0.05), but the IOP in the treatment group was higher than that in the normal control group. The IOP in the treatment group was lower than that in the chronic high intraocular pressure group on the following 7 days and 14 days. However, the IOP was still higher than that in the normal control group, and the difference was significant (P 0.05). 2. Histological changes of chronic intraocular hypertension were retinal nerve fiber layer and edema of internal plexiform layer. Late retinal inner layer edema subsided, atrophy, thinning, retinal ganglion cells decreased. Compared with chronic high intraocular pressure group, edema subsided more quickly, atrophy was not obvious and the number of retinal ganglion cells decreased significantly in the treatment group than in the chronic high intraocular pressure group. Results of 3.RGCs count: there was no significant difference in the number of RGCs between the treatment group and the chronic high intraocular pressure group before treatment and 1 day after treatment (P 0.05), but the number of RGCs in the treatment group was lower than that in the normal control group. The number of RGCs in the chronic intraocular hypertension group was significantly lower than that in the treatment group on the 7th and 14th day after the treatment, and the difference was significant (P 0.05). But the number of the treatment group was still less than that of the normal control group, and the difference was significant (P 0.05). 4. Immunohistochemical observation showed that GAP-43 was expressed in RGCsof retinal nerve fiber layer and on the inner plexiform layer. The expression of GAP-43 in chronic intraocular pressure group was increased at the early stage, then decreased gradually, and then decreased gradually, but the expression of GAP-43 was increased in the treatment group at the early stage, and increased steadily during the observation period. There was a significant difference between different periods (P 0.05). Conclusion: 1. Pathological and intraocular pressure changes showed that the model of chronic high intraocular pressure was successfully established in mice. 2.LIF increased the expression of GAP-43 in mice with chronic intraocular hypertension. 3.LIF can protect retinal ganglion cells from chronic intraocular hypertension in mice.
【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2011
【分類號(hào)】：R775

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