Abstract：
OBJECTIVE: Methylglyoxal (MG) is the most potent precursor during the formation of the advanced glycation end products (AGEs). MG-dependent glycative stress contributes to pathogenesis of diabetes, age-related disorders, and cancer. There is a great need to study the reduction process of glycative stress for effective management of metabolic disorders. From natural compounds to synthetic drugs, each element contributes to the reduction of glycative stress. Previously, it was established that the lowering of uric acid, low-density lipoprotein cholesterol, and urine albumin excretion rate, as well as reducing total oxidative stress, were all achieved more effectively with a levothyroxine regimen. Still, there is no such study found that supports the MG-dependent glycative stress reduction with thyroid hormone compound. Our study aims to investigate the effects of T3 and T4 on MG-dependent glycative stress.
METHODS: The antiglycation effect was assayed through NBT assay, DNPH assay, ELISA, and fluorescence spectrophotometer. The intracellular reduction in reactive oxygen species (ROS) has been estimated through confocal microscopy.
RESULTS: The results revealed an effective reduction in the formation of AGEs adducts and intracellular ROS formation.
CONCLUSIONS: The investigation concludes AGEs formation was suppressed using these compounds, although in vivo and rigorous clinical trials are required in order to verify these findings.
METHODS: The antiglycation effect was assayed through NBT assay, DNPH assay, ELISA, and fluorescence spectrophotometer. The intracellular reduction in reactive oxygen species (ROS) has been estimated through confocal microscopy.
RESULTS: The results revealed an effective reduction in the formation of AGEs adducts and intracellular ROS formation.
CONCLUSIONS: The investigation concludes AGEs formation was suppressed using these compounds, although in vivo and rigorous clinical trials are required in order to verify these findings.
摘要：
目的：甲基乙二醛（MG）是晚期糖基化终产物（AGEs）形成过程中最有效的前体。MG依赖性糖基化应激有助于糖尿病的发病机制，与年龄有关的疾病，和癌症。非常需要研究糖化应激的减少过程以有效管理代谢紊乱。从天然化合物到合成药物，每个元素都有助于减少糖化应激。以前,已经确定降低尿酸，低密度脂蛋白胆固醇，和尿白蛋白排泄率，以及减少总氧化应激，使用左甲状腺素方案均可更有效地实现。尽管如此，没有这样的研究发现支持使用甲状腺激素化合物减少MG依赖性的糖化应激。我们的研究旨在探讨T3和T4对MG依赖性糖化应激的影响。
方法：用NBT法检测抗糖基化作用,DNPH测定,ELISA,和荧光分光光度计。通过共聚焦显微镜估计了细胞内活性氧（ROS）的减少。
结果：结果显示有效减少了AGEs加合物的形成和细胞内ROS的形成。
结论：研究结论使用这些化合物抑制了AGEs的形成，尽管为了验证这些发现，需要进行体内和严格的临床试验。
方法：用NBT法检测抗糖基化作用,DNPH测定,ELISA,和荧光分光光度计。通过共聚焦显微镜估计了细胞内活性氧（ROS）的减少。
结果：结果显示有效减少了AGEs加合物的形成和细胞内ROS的形成。
结论：研究结论使用这些化合物抑制了AGEs的形成，尽管为了验证这些发现，需要进行体内和严格的临床试验。
