The Protective Effect of EGCG on INS-1 Cell in the Oxidative Stress and Mechanism.
10.4093/kdj.2008.32.2.121
- Author:
Mi Kyung KIM
1
;
Hye Sook JUNG
;
Chang Shin YOON
;
Min Jeong KWON
;
Kyung Soo KOH
;
Byung Doo RHEE
;
Jeong Hyun PARK
Author Information
1. Maryknoll General Hospital, Korea.
- Publication Type:Original Article
- Keywords:
Antiapoptosis;
Antioxidant;
EGCG;
INS cell;
Oxidative stress
- MeSH:
Androstadienes;
Blotting, Western;
Catalase;
Diabetes Complications;
Glutathione;
Glutathione Peroxidase;
Hydrogen Peroxide;
Insulin;
Insulin-Secreting Cells;
Oxidative Stress;
Tea
- From:Korean Diabetes Journal
2008;32(2):121-130
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Oxidative stress is important in both diabetic complications and the development and the progression of type 2 diabetes via the effects on the pancreatic beta-cells. EGCG (epigallocatechin galleate), a major constituent of green tea, has been known to have beneficial effects on various diseases through the mechanisms of antioxidant and cell signaling modulation. But, very small numbers of studies were published about the direct effects of EGCG on the pancreatic beta cell lines. We performed this study to see the protective effect of EGCG on pancreatic beta cell line under H2O2 and the mechanisms of this phenomenon. METHODS: We used INS-1 cells and hydrogen peroxide as an oxidative stressor. Their viabilities were verified by MTT assay and FACS. The activity of glutathione peroxidase was assessed by total glutathione quantification kit. Western blot and semi-quantitative RT-PCR for the catalase, SOD (superoxide dismutase), PI3K and Akt were performed. Functional status of INS-1 cells was tested by GSIS (glucose stimulated insulin secretion). RESULTS: The biological effects of EGCG were different according to its concentrations. 10 micrometer EGCG effectively protected hydrogen peroxide induced damage in INS-1 cells. The expression and the activity of SOD, catalase and the glutathione peroxidase were significantly increased by EGCG. EGCG significantly increased PI3K and Akt activity and its effect was inhibited partially by wortmannin. GSIS was well preserved by EGCG. CONCLUSION: EGCG in low concentration effectively protected INS-1 cells from the oxidative stress through the activation of both antioxidant systems and anti-apoptosis signaling. Further studies will be necessary for the more detailed mechanisms and the clinical implications.
