大鼠慢性高眼压视网膜NogoA的表达_临床医学论文.docVIP

大鼠慢性高眼压视网膜NogoA的表达_临床医学论文.doc

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大鼠慢性高眼压视网膜NogoA的表达_临床医学论文.doc

大鼠慢性高眼压视网膜Nogo的表达_临床医学论文 大鼠慢性高眼压视网膜Nogo的表达_临床医学论文 作者:聂庆珠,刘致力,沙倩,高殿文 【摘要】   目的:研究慢性高眼压大鼠视网膜髓鞘相关抑制蛋白Nogo表达的变化。 方法:成年雄性Wistar大鼠36只随机分为正常对照组6只和慢性高眼压组30只,应用免疫组织化学方法观察慢性高眼压大鼠视网膜不同时点Nogo表达的变化。结果:与正常对照组相比,慢性高眼压21d大鼠视网膜变薄,节细胞数量减少(0.05); Nogo表达增多,与形态学变化相一致(0.05)。结论:髓鞘相关抑制蛋白Nogo在慢性高眼压大鼠视网膜损伤过程中发挥了重要作用。 【关键词】 视网膜;慢性高眼压;Nogo;视网膜神经节细胞  Abstractgroup (6 rats) and chronic hypertension group (30 rats). Chronic hypertension was created by cauterizing the superficial scleral veins. Immunohistochemistry technique was used to evaluate the expressive varieties of NogoA at different time points during the course of chronic ocular hypertension.RESULTS: The success of the model was indicated by over 40% of increase in the IOP as compared with normal rats. Compared with control group, as time passed chronic hypertension group gradually had detectable morphology changes in the retina. At the 21st day of chronic ocular hypertension, retinas became thinner and the quantity of retinal ganglion cell (RGC) decreased (0.05). Assoicated with the morphological changes, the expression of NogoA was strongly increased (0.05).CONCLUSION: Myelin associated protein NogoA plays a part in the process of chronic ocular hypertension.   KEYWORDS: retina; chronic hypertension; Nogo   INTRODUCTION   The pathological mechanism of glaucomatous optic neuropathy is progressive death of retinal ganglion cells, which leads to irreversible damage. Regeneration of damaged central nervous system, including optic nerve, is difficult to achieve because of a number of reasons, such as inhibitors of axonal regeneration are present in myelin, lack of neurotrophic factors, and formation of the glia scar. It has been postulated that the regeneration of central nervous system is affected by myelin associated protein NogoA. NogoA, which is predominantly present in oligodendrocytes and myelin in the adult central nervous system (CNS), not only restricts neurite growth, plasticity, and axonal regeneration, but also limits the

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