Preventative Effects of 4,4'‐Diphenylmethane‐bis(methyl) Carbamate Isolated from Cortex Mori on Human Umbilical Vein Endothelial Cell Dysfunction Induced by Advanced Glycation End Products
2012
Feng, Liang | Xu, You‐hua | Wang, Shan‐shan | Au‐yeung, Wai | Zheng, Zhao‐guang | Wang, Ru‐shang | Zhu, Quan | Xiang, Ping
Advanced glycation end‐products (AGEs) have been regarded as an initial motivating factor in the pathogenesis of endothelial dysfunction in diabetic complications. 4,4'‐Diphenylmethane‐bis(methyl) carbamate (DMPC), a carbamate compound, was isolated from Cortex Mori and its prevention effects against AGEs‐induced endothelial dysfunction were studied. 4,4'‐Diphenylmethane‐bis(methyl) carbamate significantly reduced cell apoptosis to normal level at 10−9 mol/L concentration. Advanced glycation end‐products up‐regulated the expression of Bad and Bax and down‐regulated Bcl‐2 proteins, and pretreatment with DMPC significantly down‐regulated Bad and Bax while up‐regulating Bcl‐2 expressions. In addition, ICAM (intercellular adhesion molecule)‐1 and TGF (transforming growth factor)‐β1 expressions in human umbilical vein endothelial cell (HUVEC) were significantly enhanced by AGEs. More importantly, these increases of ICAM‐1 and TGF‐β1 expressions were reduced meaningfully with the pretreatment of DMPC. All the results showed DMPC had prevention effects against the progression of AGE‐induced endothelial dysfunction, and this compound might be a promising agent against endothelial dysfunction in diabetic vascular complications.
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