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首页> 外文期刊>Iranian Journal of Medical Sciences >Melatonin Reduces Cataract Formation and Aldose Reductase Activity in Lenses of Streptozotocin-induced Diabetic Rat
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Melatonin Reduces Cataract Formation and Aldose Reductase Activity in Lenses of Streptozotocin-induced Diabetic Rat

机译:褪黑素减少链脲佐菌素诱导的糖尿病大鼠晶状体的白内障形成和醛糖还原酶活性

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Background: The relationship between the high activity of aldose reductase (AR) and diabetic cataract formation has been previously investigated. The purpose of the present study was to determine the preventing effect of melatonin on streptozotocin (STZ)-induced diabetic cataract in rats. Methods: 34 adult healthy male Sprague-Dawely rats were divided into four groups. Diabetic control and diabetic+melatonin received a single dose of STZ (50 mg/kg, intraperitoneally), whereas the normal control and normal+melatonin received vehicle. The melatonin groups were gavaged with melatonin (5 mg/kg) daily for a period of 8 weeks, whereas the rats in the normal control and diabetic control groups received only the vehicle. The rats’ eyes were examined every week and cataract formation scores (0-4) were determined by slit-lamp microscope. At the end of the eighth week, the rats were sacrificed and markers of the polyol pathway and antioxidative (Glutathione, GSH) in their lens were determined. The levels of blood glucose, HbA1c and plasma malondialdhyde (MDA), as a marker of lipid peroxidation, were also measured. Results: Melatonin prevented STZ-induced hyperglycemia by decreased blood glucose and HbA1c levels. Slit lamp examination indicated that melatonin delayed cataract progression in diabetic rats. The results revealed that melatonin feeding increased the GSH levels, decreased the activities of AR and sorbitol dehydrogenase (SDH) and sorbitol formation in catractous lenses as well as plasma MDA content. Conclusion: In summary, for the first time we demonstrated that melatonin delayed the formation and progression of cataract in diabetic rat lenses.
机译:背景:醛糖还原酶(AR)的高活性与糖尿病性白内障形成之间的关系已有研究。本研究的目的是确定褪黑素对链脲佐菌素(STZ)诱导的糖尿病性白内障的预防作用。方法:将34只成年健康雄性Sprague-Dawely大鼠分为四组。糖尿病对照组和糖尿病+褪黑激素接受单剂量的STZ(50 mg / kg,腹膜内),而正常对照组和正常+褪黑激素则接受媒介物。褪黑激素组每天用褪黑激素(5 mg / kg)灌胃,持续8周,而正常对照组和糖尿病对照组的大鼠仅接受载体。每周检查大鼠的眼睛,并用裂隙灯显微镜测定白内障形成分数(0-4)。在第八周结束时,处死大鼠并测定其晶状体中多元醇途径和抗氧化的标记物(谷胱甘肽,GSH)。还测量了血糖,HbA1c和血浆丙二醛(MDA)的水平,作为脂质过氧化的标志物。结果:褪黑素通过降低血糖和HbA1c水平来预防STZ诱导的高血糖症。裂隙灯检查表明褪黑素延迟了糖尿病大鼠的白内障进展。结果表明,褪黑激素喂养增加了谷胱甘肽水平,降低了活动性晶状体中AR和山梨醇脱氢酶(SDH)的活性和山梨醇的形成以及血浆MDA含量。结论:总之,我们首次证明褪黑素能延迟糖尿病大鼠晶状体白内障的形成和发展。

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