在1型糖尿病大鼠模型中,尼古丁暴露加剧了白内障的发展。

Experimental Diabetes Research Pub Date : 2012-01-01 Epub Date: 2012-09-20 DOI:10.1155/2012/349320
Nima Tirgan, Gabriela A Kulp, Praveena Gupta, Adam Boretsky, Tomasz A Wiraszka, Bernard Godley, Ronald G Tilton, Massoud Motamedi
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引用次数: 12

摘要

糖尿病和吸烟是白内障发展的危险因素。在这项研究中,我们评估了尼古丁对1型糖尿病大鼠模型白内障进展的影响。单次注射链脲佐菌素65 mg/kg诱导sd大鼠糖尿病。每日皮下注射尼古丁。45只大鼠被分成两组,一组是接受和不接受尼古丁治疗的糖尿病患者,另一组是接受和不接受尼古丁治疗的对照组。使用裂隙灯生物显微镜监测晶状体混浊的进展并进行评分。为了评估全身性炎症是否在介导白内障发生中起作用,我们研究了eotaxin、IL-6和IL-4的血清水平。测量的细胞因子水平在尼古丁治疗和未治疗的糖尿病动物中与对照组相比显著增加,并且在尼古丁治疗的糖尿病大鼠中显示出积极的趋势。我们的数据表明尼古丁和糖尿病之间存在协同关系,通过炎症介质加速白内障的形成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Nicotine exposure exacerbates development of cataracts in a type 1 diabetic rat model.

Diabetes and smoking are known risk factors for cataract development. In this study, we evaluated the effect of nicotine on the progression of cataracts in a type 1 diabetic rat model. Diabetes was induced in Sprague-Dawley rats by a single injection of 65 mg/kg streptozotocin. Daily nicotine injections were administered subcutaneously. Forty-five rats were divided into groups of diabetics with and without nicotine treatment and controls with and without nicotine treatment. Progression of lens opacity was monitored using a slit lamp biomicroscope and scores were assigned. To assess whether systemic inflammation played a role in mediating cataractogenesis, we studied serum levels of eotaxin, IL-6, and IL-4. The levels of the measured cytokines increased significantly in nicotine-treated and untreated diabetic animals versus controls and demonstrated a positive trend in the nicotine-treated diabetic rats. Our data suggest the presence of a synergistic relationship between nicotine and diabetes that accelerated cataract formation via inflammatory mediators.

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来源期刊
Experimental Diabetes Research
Experimental Diabetes Research 医学-内分泌学与代谢
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