Effect of allithiamine on the level of hyperglycaemia-induced advanced glycation end products

Diabetes mellitus is a rapidly growing public health burden in both developed and developing countries. Diabetes mellitus is accompanied by hyperglycaemia, which can cause tissue injury by several mechanisms. One of these is the formation of advanced glycation end-products (AGEs). In this study, the effect of allithaimine, a fat-soluble thiamine derivative, was investigated on hyperglycaemia-induced AGEs levels using human umbilical cord vein endothelial cells (HUVECs) as a hyperglycaemic model. HUVECs were isolated by enzymatic digestion, characterized by flow cytometer and treated 30 mM glucose plus allithaimine or thiamine or cell maintenance medium as control. Allithiamine was synthesized and purified. The structure of the synthesized and isolated compound was verified by reverse phase HPLC and MALDI-TOF. AGEs were evaluated by ELISA. Collectively, our results indicate that allithiamine can reduce level of the hyperglycaemia-induced AGEs similar to thiamine.

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Advanced Glycation End Products: A Link Between Periodontitis and Diabetes Mellitus?

Current Diabetes Reviews ◽

10.2174/15733998113099990066 ◽

2013 ◽

Vol 9 (5) ◽

pp. 355-361 ◽

Cited By ~ 29

Author(s):

Abhijit Gurav

Keyword(s):

Diabetes Mellitus ◽

Advanced Glycation End Products ◽

Advanced Glycation ◽

Glycation End Products ◽

End Products

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Advanced glycation end products induce a prothrombotic phenotype in mice via interaction with platelet CD36

Blood ◽

10.1182/blood-2011-10-387506 ◽

2012 ◽

Vol 119 (25) ◽

pp. 6136-6144 ◽

Cited By ~ 62

Author(s):

Weifei Zhu ◽

Wei Li ◽

Roy L. Silverstein

Keyword(s):

Diabetes Mellitus ◽

Mouse Models ◽

Advanced Glycation End Products ◽

Vascular Complications ◽

Dependent Manner ◽

Advanced Glycation ◽

Drug Induced ◽

Glycation End Products ◽

End Products

Abstract Diabetes mellitus has been associated with platelet hyperreactivity, which plays a central role in the hyperglycemia-related prothrombotic phenotype. The mechanisms responsible for this phenomenon are not established. In the present study, we investigated the role of CD36, a class-B scavenger receptor, in this process. Using both in vitro and in vivo mouse models, we demonstrated direct and specific interactions of platelet CD36 with advanced glycation end products (AGEs) generated under hyperglycemic conditions. AGEs bound to platelet CD36 in a specific and dose-dependent manner, and binding was inhibited by the high-affinity CD36 ligand NO2LDL. Cd36-null platelets did not bind AGE. Using diet- and drug-induced mouse models of diabetes, we have shown that cd36-null mice had a delayed time to the formation of occlusive thrombi compared with wild-type (WT) in a FeCl3-induced carotid artery injury model. Cd36-null mice had a similar level of hyperglycemia and a similar level of plasma AGEs compared with WT mice under this condition, but WT mice had more AGEs incorporated into thrombi. Mechanistic studies revealed that CD36-dependent JNK2 activation is involved in this prothrombotic pathway. Therefore, the results of the present study couple vascular complications in diabetes mellitus with AGE-CD36–mediated platelet signaling and hyperreactivity.

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