請用此 Handle URI 來引用此文件: http://hdl.handle.net/11455/62188
標題: Inhibitory effect of vanillic acid on methylglyoxal-mediated glycation in apoptotic Neuro-2A cells
作者: Huang, S.M.
顏國欽
Hsu, C.L.
Chuang, H.C.
Shih, P.H.
Wu, C.H.
Yen, G.C.
關鍵字: CML
Methylglyoxal
Apoptosis
Vanillic acid
Diabetic neuropathy
Neuro-2A cells
protein-kinase-c
experimental diabetic-neuropathy
glucose-induced
apoptosis
n-terminal kinase
rat schwann-cells
oxidative stress
maillard reaction
complications
activation
expression
期刊/報告no:: Neurotoxicology, Volume 29, Issue 6, Page(s) 1016-1022.
摘要: Methylglyoxal is a reactive dicarbonyl compound generated as an intermediate of glycolysis during the physical glycation in the diabetic condition. It is considered to be a potent precursor of advanced glycation end products (AGES) formation. Methylglyoxal itself and methylglyoxal-derived AGES have been commonly implicated in the development of diabetic neuropathy. Our previous study indicated that vanillic acid showed an inhibitory effect against methylglyoxal-mediated Neuro-2A cell apoptosis, suggesting that vanillic acid might possess cytoprotective properties in the prevention of diabetic neuropathy complication. In this study, the effects of vanillic acid on the methylglyoxal-mediated glycation system involved in the progression of Neuro-2A cell apoptosis were further investigated. Our findings indicated that methylglyoxal-induced Neuro-2A cell apoptosis was mediated through the possible glycation mechanism of oxidative stress, activation of the MAPK signaling pathway (p38 and JNK) and oxidation-sensitive protein expression (PKC and p47(phox)) and methylglyoxal-derived N-epsilon-(carboxymethyl)lysine (CIVIL) formation. Vanillic acid, however, suppressed methylglyoxal-induced Neuro-2A cell apoptosis via inhibition of glycation mechanisms including ROS, p38 and JNK, PKC and p47(phox), and methylglyoxal-derived CML formation. In the present study, we established the first evidence that vanillic acid might contribute to the prevention of the development of diabetic neuropathy by blocking the methylglyoxal-mediated intracellular glycation system. (c) 2008 Elsevier Inc. All rights reserved.
URI: http://hdl.handle.net/11455/62188
ISSN: 0161-813X
文章連結: http://dx.doi.org/10.1016/j.neuro.2008.07.002
顯示於類別:食品暨應用生物科技學系

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