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光诱导的视网膜病变幼鼠模型的研究

发布时间:2018-05-01 11:13

  本文选题:光损伤 + 视网膜电生理图 ; 参考:《浙江大学》2010年硕士论文


【摘要】: 研究背景和目的:视网膜是感受光线形成视觉的主要器官,它由不同的细胞层组成的,可分为视网膜外层和视网膜内层。视细胞膜富含多不饱和脂肪酸,特别是DHA,这使得在感光换能过程中起主要作用的视细胞外段对脂质的过氧化非常敏感。另外,视网膜外层无血管结构,只能通过蛛网膜与外界进行物质交换,对视细胞的代谢产生影响。视网膜的这些特点使其对氧化压力的耐受性很低。 强光照射会使视网膜中的视细胞产生大量氧化产物和自由基,过度的氧化压力会引起视细胞凋亡,进一步导致视网膜结构和功能的退化,这种现象称为光诱导的视网膜病变。随着视网膜的成熟和衰老,其细胞活性下降,自我调节能力降低,可塑性变差。因此,成熟视网膜和发育中的视网膜对光损伤的反应大不相同。有研究表明,幼年大鼠的视网膜对光损伤有抵制作用。 新生大鼠模型为研究人类在胎儿期的初级视觉通路的发育提供的范例。研究新生大鼠的视网膜光损伤过程及其保护机制,可进一步阐明某些人类视网膜疾病的发生和发展过程,并为诊断和治疗提供理论基础。 实验方法:Sprague Dawley大鼠在出生后14到28天在10000 lux的强度下饲养14天,之后移入正常环境。在幼鼠出生后30天到60天每隔5天对其进行视网膜电生理图检测、视觉激发点位检测和多焦点视网膜电生理图检测,并取其视网膜做组织学观察和CNFT含量测定。 实验结果:光照使幼鼠视网膜功能下降,但从P30到P40其功能有所恢复,之后逐步下降到P30水平。视网膜结构在结束光照后发生退化,尤其是视网膜外层的厚度,明显下降,而内层厚度与正常无显著差异。视网膜在光照结束后初期显示出视盘的再生长,生长期约为10天。大脑的视觉上皮的电信号没有显示出明显的衰减。上下视网膜视网膜外核层厚度分布不均,上视网膜有一个特定区域受损特别严重。上下视网膜在光照后其睫状体神经营养因子(CNTF)的含量不同,上视网膜明显高于下视网膜。 结论:幼鼠的光损伤模型是一个逐步发展的退化过程,分为急性期和慢性期。上视网膜有个特定区域对光十分敏感,受到光损伤的程度最深,这导致上视网膜中CNTF的含量明显上调。因此,视细胞的凋亡程度可能是调节生长因子分泌情况的因素之一。
[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.
【学位授予单位】:浙江大学
【学位级别】:硕士
【学位授予年份】:2010
【分类号】:R774.1

【共引文献】

相关期刊论文 前1条

1 梁洁;陈鹏;闫文华;马萍;方毅;康宏向;高荣莲;王长振;;氦氖激光辐照致眼损伤的机制研究[J];职业与健康;2013年06期

相关博士学位论文 前1条

1 方家华;双七他克林对大鼠视网膜神经节细胞兴奋性毒素损伤的保护作用及机制研究[D];华中科技大学;2010年

相关硕士学位论文 前2条

1 王晓英;激光视网膜损伤中M(?)ller细胞—神经元相互作用的研究[D];中国人民解放军军事医学科学院;2004年

2 尹澜;笃斯越橘对兔视网膜光损伤后组织结构及功能的保护作用[D];中国人民解放军军医进修学院;2010年



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