Khorsand Marjan, Akmali Masoumeh, Sharzad Sahab, Beheshtitabar Mojtaba
Department of Biochemistry and Molecular Biology, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Department of Biochemistry, Shiraz University of Medical Sciences, Shiraz, Iran.
Iran J Med Sci. 2016 Jul;41(4):305-13.
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.
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.
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.
In summary, for the first time we demonstrated that melatonin delayed the formation and progression of cataract in diabetic rat lenses.
醛糖还原酶（AR）活性升高与糖尿病性白内障形成之间的关系此前已被研究。本研究的目的是确定褪黑素对链脲佐菌素（STZ）诱导的大鼠糖尿病性白内障的预防作用。
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+褪黑素组腹腔注射单剂量STZ（50mg/kg），而正常对照组和正常+褪黑素组注射溶剂。褪黑素组每天灌胃褪黑素（5mg/kg），持续8周，而正常对照组和糖尿病对照组的大鼠仅接受溶剂。每周检查大鼠眼睛，并用裂隙灯显微镜确定白内障形成评分（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（谷胱甘肽，GSH）的标志物。还测量了血糖、糖化血红蛋白（HbA1c）和血浆丙二醛（MDA）水平，MDA作为脂质过氧化的标志物。
褪黑素通过降低血糖和HbA1c水平预防STZ诱导的高血糖。裂隙灯检查表明，褪黑素延缓了糖尿病大鼠白内障的进展。结果显示，喂食褪黑素可提高GSH水平，降低白内障晶状体中AR和山梨醇脱氢酶（SDH）的活性以及山梨醇的形成，同时降低血浆MDA含量。
总之，我们首次证明褪黑素延缓了糖尿病大鼠晶状体白内障的形成和进展。
