發(fā)布時間：2018-05-01 11:13

  本文選題：光損傷 + 視網(wǎng)膜電生理圖　； 參考：《浙江大學(xué)》2010年碩士論文

【摘要】： 研究背景和目的：視網(wǎng)膜是感受光線形成視覺的主要器官,它由不同的細胞層組成的,可分為視網(wǎng)膜外層和視網(wǎng)膜內(nèi)層。視細胞膜富含多不飽和脂肪酸,特別是DHA,這使得在感光換能過程中起主要作用的視細胞外段對脂質(zhì)的過氧化非常敏感。另外,視網(wǎng)膜外層無血管結(jié)構(gòu),只能通過蛛網(wǎng)膜與外界進行物質(zhì)交換,對視細胞的代謝產(chǎn)生影響。視網(wǎng)膜的這些特點使其對氧化壓力的耐受性很低。 強光照射會使視網(wǎng)膜中的視細胞產(chǎn)生大量氧化產(chǎn)物和自由基,過度的氧化壓力會引起視細胞凋亡,進一步導(dǎo)致視網(wǎng)膜結(jié)構(gòu)和功能的退化,這種現(xiàn)象稱為光誘導(dǎo)的視網(wǎng)膜病變。隨著視網(wǎng)膜的成熟和衰老,其細胞活性下降,自我調(diào)節(jié)能力降低,可塑性變差。因此,成熟視網(wǎng)膜和發(fā)育中的視網(wǎng)膜對光損傷的反應(yīng)大不相同。有研究表明,幼年大鼠的視網(wǎng)膜對光損傷有抵制作用。 新生大鼠模型為研究人類在胎兒期的初級視覺通路的發(fā)育提供的范例。研究新生大鼠的視網(wǎng)膜光損傷過程及其保護機制,可進一步闡明某些人類視網(wǎng)膜疾病的發(fā)生和發(fā)展過程,并為診斷和治療提供理論基礎(chǔ)。 實驗方法：Sprague Dawley大鼠在出生后14到28天在10000 lux的強度下飼養(yǎng)14天,之后移入正常環(huán)境。在幼鼠出生后30天到60天每隔5天對其進行視網(wǎng)膜電生理圖檢測、視覺激發(fā)點位檢測和多焦點視網(wǎng)膜電生理圖檢測,并取其視網(wǎng)膜做組織學(xué)觀察和CNFT含量測定。 實驗結(jié)果：光照使幼鼠視網(wǎng)膜功能下降,但從P30到P40其功能有所恢復(fù),之后逐步下降到P30水平。視網(wǎng)膜結(jié)構(gòu)在結(jié)束光照后發(fā)生退化,尤其是視網(wǎng)膜外層的厚度,明顯下降,而內(nèi)層厚度與正常無顯著差異。視網(wǎng)膜在光照結(jié)束后初期顯示出視盤的再生長,生長期約為10天。大腦的視覺上皮的電信號沒有顯示出明顯的衰減。上下視網(wǎng)膜視網(wǎng)膜外核層厚度分布不均,上視網(wǎng)膜有一個特定區(qū)域受損特別嚴重。上下視網(wǎng)膜在光照后其睫狀體神經(jīng)營養(yǎng)因子(CNTF)的含量不同,上視網(wǎng)膜明顯高于下視網(wǎng)膜。 結(jié)論：幼鼠的光損傷模型是一個逐步發(fā)展的退化過程,分為急性期和慢性期。上視網(wǎng)膜有個特定區(qū)域?qū)馐置舾?受到光損傷的程度最深,這導(dǎo)致上視網(wǎng)膜中CNTF的含量明顯上調(diào)。因此,視細胞的凋亡程度可能是調(diào)節(jié)生長因子分泌情況的因素之一。
[Abstract]:Background and objective: the retina is the main organ of light-forming vision. It is composed of different cellular layers and can be divided into the outer layer of the retina and the inner layer of the retina. The apparent cell membrane is rich in polyunsaturated fatty acids, especially DHA, which makes the extracellular segment which plays an important role in the photo-transduction process very sensitive to lipid peroxidation. In addition, there is no vascular structure in the outer layer of the retina, which can only exchange substances with the outside through arachnoid, which has an effect on the metabolism of the visual cells. These characteristics of the retina make it low tolerance to oxidative pressure. Strong light irradiation can produce a large number of oxidation products and free radicals in the retinal cells. Excessive oxidative pressure will lead to apoptosis of the retinal cells and further degenerate the structure and function of the retina. This phenomenon is called photoinduced retinopathy. With the maturation and senescence of retina, the cell activity, self-regulation ability and plasticity of retina decrease. As a result, the response of mature and developing retina to light damage is very different. Studies have shown that the retina of young rats can resist light damage. The neonatal rat model provides an example for studying the development of primary visual pathways in human fetuses. To study the process of retinal light damage and its protective mechanism in neonatal rats can further elucidate the occurrence and development of some human retinal diseases and provide a theoretical basis for diagnosis and treatment. Methods: Sprague Dawley rats were fed at 10000 lux for 14 to 28 days after birth, and then transferred to normal environment. From 30 to 60 days after birth, the electroretinogram, the visual excitation point and the multifocal electroretinogram were detected every 5 days after birth, and their retina was taken for histological observation and CNFT content determination. The results showed that the retinal function of young rats was decreased by light, but it recovered from P30 to P40, and then gradually decreased to P30 level. The retinal structure degenerated after illumination, especially the thickness of the outer layer of the retina decreased significantly, but the thickness of the inner layer was not significantly different from that of the normal. The retina shows the regrowth of the optic disc in the early stage after illumination, and the growth period is about 10 days. Electrical signals from the visual epithelium of the brain do not show significant attenuation. The thickness of the outer nuclear layer of the upper and lower retina is unevenly distributed, and a specific area of the upper retina is severely damaged. The content of CNTFs in the upper and lower retina was significantly higher than that in the lower retina. Conclusion: the model of light injury in young rats is a progressive and degenerative process, which is divided into acute stage and chronic stage. There is a specific area of the upper retina that is sensitive to light and is most damaged by light, which leads to a significant increase in the content of CNTF in the upper retina. Therefore, the degree of apoptosis may be one of the factors regulating the secretion of growth factor.
【學(xué)位授予單位】：浙江大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2010
【分類號】：R774.1

【共引文獻】

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2 尹瀾;篤斯越橘對兔視網(wǎng)膜光損傷后組織結(jié)構(gòu)及功能的保護作用[D];中國人民解放軍軍醫(yī)進修學(xué)院;2010年

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本文編號：1829093