Document Detail


Cytoprotective effects of phenolic acids on methylglyoxal-induced apoptosis in Neuro-2A cells.
MedLine Citation:
PMID:  18481334     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In the process of glycation, methylglyoxal is a reactive dicarbonyl compound physiologically generated as an intermediate of glycolysis, and is found in high levels in blood or tissue of diabetic models. Biological glycation has been commonly implicated in the development of diabetic microvascular complications of neuropathy. Increasing evidence suggests that neuronal cell cycle regulatory failure followed by apoptosis is an important mechanism in the development of diabetic neuropathy complication. Naturally occurring antioxidants, especially phenolic acids have been recommended as the major bioactive compounds to prevent chronic diseases and promote health benefits. The objective of this study was to investigate the inhibitory abilities of phenolic acids (chlorogenic acid, syringic acid and vanillic acid) on methylglyoxal-induced mouse Neuro-2A neuroblastoma (Neuro-2A) cell apoptosis in the progression of diabetic neuropathy. The data indicated that methylglyoxal induced mouse Neuro-2A neuroblastoma (Neuro-2A) cell apoptosis via alternation of mitochondria membrane potential and Bax/Bcl-2 ratio, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase. Furthermore, the results demonstrated that activation of mitogen-activated protein kinase signal pathways (JNK and p38) participated in the methylglyoxal-induced Neuro-2A cell apoptosis process. Treatment of Neuro-2A cells with phenolic acids markedly suppresses cell apoptosis induced by methylglyoxal, suggesting that phenolic acids possess cytoprotective ability in the prevention of diabetic neuropathy complication.
Authors:
Shang-Ming Huang; Hong-Chih Chuang; Chi-Hao Wu; Gow-Chin Yen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Molecular nutrition & food research     Volume:  52     ISSN:  1613-4133     ISO Abbreviation:  Mol Nutr Food Res     Publication Date:  2008 Aug 
Date Detail:
Created Date:  2008-08-26     Completed Date:  2008-10-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101231818     Medline TA:  Mol Nutr Food Res     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  940-9     Citation Subset:  IM    
Affiliation:
Department of Food Science and Biotechnology, National Chung Hsing University, Taichung, Taiwan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects*
Caspase 3 / metabolism
Cell Line, Tumor
Cell Survival / drug effects
Chlorogenic Acid / pharmacology
Cytoprotection*
Diabetic Neuropathies / prevention & control*
Gallic Acid / analogs & derivatives,  pharmacology
Hydroxybenzoic Acids / pharmacology*
L-Lactate Dehydrogenase / secretion
MAP Kinase Signaling System
Membrane Potential, Mitochondrial / drug effects
Mice
Neuroblastoma / pathology*
Poly(ADP-ribose) Polymerases / metabolism
Proto-Oncogene Proteins c-bcl-2 / analysis
Pyruvaldehyde / toxicity*
Vanillic Acid / pharmacology
Chemical
Reg. No./Substance:
0/Hydroxybenzoic Acids; 0/Proto-Oncogene Proteins c-bcl-2; 121-34-6/Vanillic Acid; 149-91-7/Gallic Acid; 29656-58-4/phenolic acid; 327-97-9/Chlorogenic Acid; 530-57-4/syringic acid; 78-98-8/Pyruvaldehyde; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 3.4.22.-/Caspase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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