The effect of high glucose on NO and O2- through endothelial GTPCH1 and NADPH oxidase.
Life Sci
; 75(26): 3185-94, 2004 Nov 12.
Article
em En
| MEDLINE
| ID: mdl-15488897
ABSTRACT
Although endothelial dysfunction deteriorates diabetic angiopathy, the mechanisms are obscure. We revealed that high glucose augmented eNOS through stimulation of eNOS mRNA in cultured BAECs. NO was decreased and O2- was increased simultaneously. NOS inhibitor, inhibited O2- release, so did NADPH oxidase inhibitor. The effects were synergistic. Both intracellular BH4 level and GTPCH1 activity were decreased by high glucose, in line with decrease of GTPCH1 mRNA. HMG-CoA reductase inhibitor, atorvastatin increased GTPCH1 mRNA and activity, and BH4 level. Conclusively, high glucose leads to eNOS dysfunction by inhibiting BH4 synthesis and atorvastatin stimulate BH4 synthesis directly, and it may work as atherogenic process.
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Base de dados:
MEDLINE
Assunto principal:
Biopterinas
/
RNA Mensageiro
/
Regulação Enzimológica da Expressão Gênica
/
Óxido Nítrico Sintase
/
Células Endoteliais
/
Glucose
Limite:
Animals
Idioma:
En
Ano de publicação:
2004
Tipo de documento:
Article