Effects of Epigallocatechin-3-Gallate on the Expression of TGF-beta1, PKC alpha/betaII, and NF-kappaB in High-Glucose-Stimulated Glomerular Epithelial Cells / 전남의대학술지
Chonnam Medical Journal
;
: 116-121, 2011.
Artigo
em Inglês
| WPRIM
| ID: wpr-788199
ABSTRACT
Epigallocatechin-3-gallate (EGCG) is the most potent antioxidant polyphenol in green tea. In the present study, we investigated whether EGCG plays a role in the expression of transforming growth factor-beta1 (TGF-beta1), protein kinase C (PKC) alpha/betaII, and nuclear factor-kappaB (NF-kappaB) in glomerular epithelial cells (GECs) against high-glucose injury. Treatment with high glucose (30 mM) increased reactive oxygen species (ROS)/lipid peroxidation (LPO) and decreased glutathione (GSH) in GECs. Pretreatment with 100 microM EGCG attenuated the increase in ROS/LPO and restored the levels of GSH, whereas ROS, LPO, and GSH levels were not affected by treatment with 30 mM mannitol as an osmotic control. Interestingly, high-glucose treatment affected 3 separate signal transduction pathways in GECs. It increased the expression of TGF-beta1, PKC alpha/betaII, and NF-kappaB in GECs, respectively. EGCG (1, 10, 100 microM) pretreatment significantly decreased the expression of TGF-beta1 induced by high glucose in a dose-dependent manner. In addition, EGCG (100 microM) inhibited the phosphorylation of PKC alpha/betaII caused by glucose at 30 mM. Moreover, EGCG (1, 10, 100 microM) pretreatment significantly decreased the transcriptional activity of NF-kappaB induced by high glucose in a dose-dependent manner. These data suggest that EGCG could be a useful factor in modulating the injury to GECs caused by high glucose.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fosforilação
/
Chá
/
Proteína Quinase C
/
Transdução de Sinais
/
Catequina
/
NF-kappa B
/
Espécies Reativas de Oxigênio
/
Células Epiteliais
/
Fator de Crescimento Transformador beta1
/
Glucose
Idioma:
Inglês
Revista:
Chonnam Medical Journal
Ano de publicação:
2011
Tipo de documento:
Artigo
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