本文選題：糖尿病 + 角膜　； 參考：《暨南大學(xué)》2012年碩士論文

【摘要】：目的：1.采用共聚焦顯微鏡對(duì)糖尿病兔角膜組織的三維立體結(jié)構(gòu)進(jìn)行活體觀察，了解糖尿病角膜組織病變的病理形成過程。2.糖尿病兔角膜組織切片HE染色，并與活體共聚焦顯微鏡的觀察結(jié)果結(jié)合起來，宏觀分析糖尿病角膜病變的發(fā)病機(jī)制。3.通過免疫組織化學(xué)方法檢測(cè)半胱氨酸天冬氨酸蛋白酶3(caspase-3)在糖尿病兔角膜組織的表達(dá)水平，，并觀察角膜細(xì)胞與caspase-3表達(dá)變化的關(guān)系，蛋白水平分析糖尿病角膜病變發(fā)病的分子機(jī)制。 方法：1.四氧嘧啶靜脈注射新西蘭兔（18只），并給予高糖高脂飼料喂養(yǎng)來復(fù)制糖尿病模型；對(duì)照組新西蘭兔（3只）給予同等劑量的生理鹽水注射，且普通飼料喂養(yǎng)。2.分別在給藥前和疾病模型建立后4w,8w,12w采用角膜共聚焦顯微鏡進(jìn)行活體觀察。3.分別在疾病模型建立后4w,8w各處死3只糖尿病兔，12w處死12只糖尿病兔和對(duì)照組3只正常新西蘭兔，角膜組織切片HE染色，顯微鏡下觀察。4.免疫組化觀察角膜組織切片Caspase-3的表達(dá)，并與共聚焦活體觀察和角膜組織切片HE染色的結(jié)果結(jié)合，綜合分析和研究糖尿病角膜病變的發(fā)病機(jī)制。 結(jié)果：1.糖尿病兔血糖增高顯著，血糖最低17.3mmol/L,最高31.2mmol/L，平均22.97±4.03mmol/L。2.隨著糖尿病模型建立時(shí)間的延長(zhǎng)，糖尿病兔角膜逐漸出現(xiàn)不同層次的上皮脫落且脫落的面積逐漸增大。前、后基質(zhì)細(xì)胞數(shù)目減少,基質(zhì)水腫，基質(zhì)細(xì)胞核出現(xiàn)形態(tài)改變。內(nèi)皮層多形性細(xì)胞增加，內(nèi)皮細(xì)胞數(shù)目減少。上皮下神經(jīng)纖維出現(xiàn)彎曲，變形等形態(tài)學(xué)改變�；|(zhì)神經(jīng)纖維分枝減少，神經(jīng)出現(xiàn)斷裂。3. Caspase-3在糖尿病兔角膜組織的上皮和基質(zhì)層都有表達(dá)，且隨著糖尿病時(shí)間延長(zhǎng)，Caspase-3表達(dá)增強(qiáng)。 結(jié)論：糖尿病血糖增高導(dǎo)致糖尿病角膜病變的發(fā)生。隨糖尿病疾病時(shí)間的延長(zhǎng)，角膜神經(jīng)纖維和角膜上皮細(xì)胞核均發(fā)生變性，且上皮細(xì)胞凋亡、脫落；角膜基質(zhì)細(xì)胞排列疏松，水腫，細(xì)胞核變形，凋亡。我們考慮糖尿病角膜上皮細(xì)胞和基質(zhì)細(xì)胞的這些病變與角膜神經(jīng)纖維變性有關(guān)。在沒有角膜神經(jīng)分布的角膜內(nèi)皮層，角膜內(nèi)皮細(xì)胞最先被觀察到出現(xiàn)細(xì)胞形態(tài)改變，暗示這可能與角膜內(nèi)皮與房水直接接觸相關(guān)。
[Abstract]:Purpose 1. A confocal microscope was used to observe the three-dimensional structure of the cornea of diabetic rabbits in vivo, and to understand the pathological process of diabetic corneal lesions. The pathological mechanism of diabetic keratopathy was analyzed macroscopically by HE staining in corneal sections of diabetic rabbits combined with the observation of confocal microscope in vivo. The expression of cysteine aspartate proteinase 3 (caspase-3) in the cornea of diabetic rabbits was detected by immunohistochemical method. The relationship between corneal cells and caspase-3 expression was observed. The protein level was used to analyze the molecular mechanism of diabetic keratopathy. Method 1: 1. Alloxan was injected intravenously into 18 New Zealand rabbits and fed with high sugar and high fat diet to make diabetic model; in the control group, 3 New Zealand rabbits were given the same dose of normal saline, and the normal diet was fed. 2. The corneal confocal microscope was used to observe in vivo before administration and at 8 weeks and 12 weeks after the establishment of the disease model. 12 diabetic rabbits and 3 normal New Zealand rabbits were killed at 4 weeks and 8 weeks after the establishment of the model. The corneal tissue sections were stained with HE and observed under microscope. The expression of Caspase-3 in corneal sections was observed by immunohistochemistry and combined with the results of confocal in vivo and HE staining in corneal sections to analyze and study the pathogenesis of diabetic keratopathy. The result is 1: 1. Diabetic rabbits had a significant increase in blood glucose, with the lowest 17.3 mmol / L and the highest 31.2 mmol / L, with an average of 22.97 鹵4.03 mmol / L. With the prolongation of the diabetic model, the corneal epithelium of diabetic rabbits gradually appeared different levels of epithelial exfoliation and the area of exfoliation gradually increased. The number of anterior and posterior stromal cells decreased, matrix edema and morphologic changes of stromal nucleus appeared. The number of endothelial cells decreased with the increase of pleomorphic cells in the endodermis. Morphologic changes such as curvature and deformation of the nerve fibers in the subepithelial region. The branching of stromal nerve fibers was decreased, and the nerve was broken. 3. Caspase-3 was expressed in corneal epithelium and stroma of diabetic rabbits, and the expression of Caspase-3 was increased with the prolongation of diabetic time. Conclusion: diabetic keratopathy is caused by hyperglycemia. With the extension of diabetic disease, corneal nerve fibers and corneal epithelial nuclei were denatured, and epithelial cells were apoptotic, and corneal stromal cells were arranged loosely, edema, deformed nucleus and apoptosis. We consider that these lesions in diabetic corneal epithelial and stromal cells are associated with corneal nerve fiber degeneration. In the corneal endothelium without corneal nerve distribution, the morphology of corneal endothelial cells was first observed, suggesting that this may be related to the direct contact between corneal endothelium and aqueous humor.
【學(xué)位授予單位】：暨南大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類號(hào)】：R772.2;R587.2

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本文編號(hào)：1917069