Chonnam Med J.
2004 Jun;40(2):71-78.
Preventive Effects of EGCG on High Glucose Induced Podocyte Damage
- Affiliations
-
- 1Department of Internal Medicine, Chonnam National University Medical School, Korea. nhk111@chonnam.ac.kr
- 2Department of Microbiology, Chonnam National University Medical School, Korea.
- 3Department of Physiology, Chonnam National University Medical School, Korea.
- 4Department of Biochemistry, Chonnam National University Medical School, Korea.
- 5Chonnam National University Research Institute of Medical Sciences, Gwangju, Korea.
- 6Department of Pediatrics, Chungbuk National University, Cheongju, Korea.
Abstract
- The pathogenesis of diabetic nephropathy associated with reactive oxygen species (ROS) system and Mitogen-Activated Protein Kinase (MAPK) activation is well-known. Although the underlying mechanisms remain incompletely understood, epigallocatechin-3-gallate (EGCG) has antioxidant effect. This study was designed to explore the effects of EGCG on angiotensin II induced podocyte injury under high glucose condition. EGCG suppress angiotensin II induced activation of MAPK activity in high glucose condition. EGCG-mediated suppression was also observed for activation of Atypical Protein Kinase C and Protein Kinase B (Akt/PKB) activity. Whole-cell membrane potentials were recorded at room temperature by using standard patch-clamp techniques. In a current clamp mode, resting membrane potential of the podocyte was -53+/-7.02 mV under control conditions. 100 nM angiotensin II depolarized the cell (n=10) to -38.5+/-6.83 mV from the control level. Our results suggest that EGCG suppress angiotensin II induced activation of MAPK and Akt/PKB activity in high glucose condition with membrane potential change in the podocyte, which is followed by activation of voltage-dependent calcium channel. Our results suggest that EGCG suppress angiotensin II induced activation of MAPK activity in high glucose condition with membrane potential change in the podocyte, which is followed by activation of voltage-dependent calcium channel.
MeSH Terms
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Angiotensin II
Antioxidants
Calcium Channels
Diabetes Mellitus
Diabetic Nephropathies
Glucose*
Membrane Potentials
Patch-Clamp Techniques
Podocytes*
Protein Kinase C
Protein Kinases
Proto-Oncogene Proteins c-akt
Reactive Oxygen Species
Angiotensin II
Antioxidants
Calcium Channels
Glucose
Protein Kinase C
Protein Kinases
Proto-Oncogene Proteins c-akt
Reactive Oxygen Species
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