Effects of Epigallocatechin-3-Gallate on the Expression of TGF-beta1, PKC alpha/betaII, and NF-kappaB in High-Glucose-Stimulated Glomerular Epithelial Cells
10.4068/cmj.2011.47.2.116
- Author:
Sung Jun PARK
1
;
Ji Min JEONG
;
Han Seong JEONG
;
Jong Seong PARK
;
Nam Ho KIM
Author Information
1. School of Mechanical Systems Engineering, Chonnam National University, Gwangju, Korea.
- Publication Type:Original Article
- Keywords:
Glomerular epithelial cell;
Epigallocatechin-3-gallate;
Transforming growth factor-beta1;
Protein kinase C alpha/betaII;
Nuclear factor-kappaB
- MeSH:
Catechin;
Epithelial Cells;
Glucose;
Glutathione;
Mannitol;
NF-kappa B;
Phosphorylation;
Protein Kinase C;
Reactive Oxygen Species;
Signal Transduction;
Tea;
Transforming Growth Factor beta1
- From:Chonnam Medical Journal
2011;47(2):116-121
- CountryRepublic of Korea
- Language:English
-
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.
