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目的 探讨鼠实验性急慢性高眼压的视网膜组织损伤机制。方法 应用前房内连续灌注生理盐水的方法制成急性高眼压鼠模型。实验后第1、2、4、5、7和10d观察视网膜反应。巩膜表浅静脉烧灼法制成慢性高眼压模型,分别于实验后1和2个月观察视网膜损害情况。用TUNEL技术和半胱胺酸天冬胺酸酶免疫组化研究法以证实视网膜细胞的凋亡机制,NADPH辅酶反应识别一氧化氮诱导的细胞。结果 急性高眼压模型的免疫组化研究证实节细胞凋亡是早期的细胞死亡,而在对照组一氧化氮合成酶在视网膜组织并不表现明显的活性。慢性高眼压模型实验提示一氧化氮合成酶活性增加,表明一氧化氮具有神经保护作用而并非仅存有细胞毒性作用。TUNEL和半胱胺酸天冬胺酸酶研究表明,凋亡开始于慢性高眼压的不同阶段。结论 了解高眼压所致的视网膜损害的机制为研究在细胞变性过程中某些物质对凋亡、一氧化氮合成酶和突触传递的影响,尤其是对研究青光眼节细胞死亡的机制提供了基础。
Objective To investigate the mechanism of experimental retinal tissue injury in rats with acute and chronic ocular hypertension. Methods Acute intraocular pressure rat model was made by continuous infusion of saline in the anterior chamber. The retinal reaction was observed on the 1st, 2nd, 4th, 5th, 7th and 10th day after the experiment. Scleral superficial temporal vein cauterization made of chronic ocular hypertension model, respectively, 1 and 2 months after the experimental retinal damage observed. TUNEL technique and cysteine aspartase immunohistochemistry were used to confirm the apoptotic mechanism of retinal cells. NADPH coenzymes were used to identify nitric oxide-induced cells. Results Immunohistochemical studies of acute ocular hypertension demonstrated that early stage cell death was observed in the synapse but not in the control group. Chronic intraocular hypertension model experiments suggest that nitric oxide synthase activity increased, indicating that nitric oxide has neuroprotective effects and not only the existence of cytotoxicity. TUNEL and cysteine aspartase studies have shown that apoptosis begins at different stages of chronic ocular hypertension. Conclusion To understand the mechanism of retinal damage caused by intraocular pressure in order to study the impact of certain substances on apoptosis, nitric oxide synthase and synaptic transmission during cell degeneration, especially for studying the mechanism of ganglion cell death basis.