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首页> 外文期刊>Clinical and experimental ophthalmology >Early electroretinographic features of streptozotocin-induced diabetic retinopathy.
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Early electroretinographic features of streptozotocin-induced diabetic retinopathy.

机译:链脲佐菌素诱导的糖尿病性视网膜病变的早期视网膜电图特征。

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BACKGROUND: This study set out to document the early electrophysiological and immunohistochemical changes that occur in the retina of experimentally induced diabetic rats. METHODS: Diabetes was induced in rats by intraperitoneal injection of 60 mg/kg of streptozotocin (STZ). Electroretinogram readings were taken monthly under either short-duration or long-duration stimuli for up to 3 months after STZ. Oscillatory potentials (OP) and the amplitudes and implicit times of a- and b-waves were analysed, and b-wave amplitudes were analysed using a Naka-Rushton fit. Scotopic a-waves were analysed with photoreceptor models, and Rmp3 (the maximum a-wave amplitude) and S (sensitivity) were calculated. Three months after STZ injection, immunohistochemistry for glial fibrillary acidic protein was performed on the retinas of the STZ-treated rats and age-matched controls. RESULTS: The implicit OP times were significantly longer in the diabetic rats as compared with the controls, and this difference was noted as early as 1 month following STZ treatment. Other electrophysiological parameters, such as OP amplitudes, a- and b-wave amplitude as well as the implicit times, did not differ from controls at this stage. The sacrificed STZ-treated rats also demonstrated marked enhancement of glial fibrillary acidic protein immunoreactivity, suggesting that at least in experimentally induced diabetic retinopathy there is increased Muller cell reactivity. CONCLUSION: The results of this study indicated that functional alterations in the retina develop rapidly after the onset of diabetes. Analysis of each electroretinogram component may be useful in further investigating the development mechanisms of diabetic retinopathy.
机译:背景:这项研究开始记录在实验诱导的糖尿病大鼠视网膜中发生的早期电生理和免疫组织化学变化。方法:腹腔注射60 mg / kg链脲佐菌素(STZ)可诱发大鼠糖尿病。视网膜电图读数是在STZ后最多3个月的短期或长期刺激下每月获取的。分析了振荡电位(OP)以及a波和b波的振幅和隐式时间,并使用Naka-Rushton拟合分析了b波振幅。用感光体模型分析暗房a波,并计算Rmp3(最大a波振幅)和S(灵敏度)。注射STZ后三个月,在经STZ治疗的大鼠和年龄匹配的对照组的视网膜上进行了神经胶质纤维酸性蛋白的免疫组织化学研究。结果:与对照组相比,糖尿病大鼠的隐性OP时间明显更长,这种差异最早可在STZ治疗后1个月发现。在此阶段,其他电生理参数(例如OP振幅,a和b波振幅以及隐式时间)与对照无差异。处死的经STZ处理的大鼠还显示出神经胶质纤维酸性蛋白免疫反应性的显着增强,这表明至少在实验诱导的糖尿病性视网膜病中,Muller细胞反应性增加。结论:这项研究的结果表明,糖尿病发作后视网膜的功能改变迅速发展。对每个视网膜电图成分的分析可能有助于进一步研究糖尿病性视网膜病的发生机制。

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