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Neuroprotective effect of (-)-epigallocatechin-3-gallate in rats when administered pre- or post-traumatic brain injury.

Abstract
Our previous study indicated that consuming (-)-epigallocatechin gallate (EGCG) before or after traumatic brain injury (TBI) eliminated free radical generation in rats, resulting in inhibition of neuronal degeneration and apoptotic death, and improvement of cognitive impairment. Here we investigated the effects of administering EGCG at various times pre- and post-TBI on cerebral function and morphology. Wistar rats were divided into five groups and were allowed access to (1) normal drinking water, (2) EGCG pre-TBI, (3) EGCG pre- and post-TBI, (4) EGCG post-TBI, and (5) sham-operated group with access to normal drinking water. TBI was induced with a pneumatic controlled injury device at 10 weeks of age. Immunohistochemistry and lipid peroxidation studies revealed that at 1, 3, and 7 days post-TBI, the number of 8-Hydroxy-2'-deoxyguanosine-, 4-Hydroxy-2-nonenal- and single-stranded DNA (ssDNA)-positive cells, and levels of malondialdehyde around the damaged area were significantly decreased in all EGCG treatment groups compared with the water group (P < 0.05). Although there was a significant increase in the number of surviving neurons after TBI in each EGCG treatment group compared with the water group (P < 0.05), significant improvement of cognitive impairment after TBI was only observed in the groups with continuous and post-TBI access to EGCG (P < 0.05). These results indicate that EGCG inhibits free radical-induced neuronal degeneration and apoptotic death around the area damaged by TBI. Importantly, continuous and post-TBI access to EGCG improved cerebral function following TBI. In summary, consumption of green tea may be an effective therapy for TBI patients.
AuthorsTatsuki Itoh, Masaki Tabuchi, Nobuyuki Mizuguchi, Motohiro Imano, Masahiro Tsubaki, Shozo Nishida, Shigeo Hashimoto, Kazuhiko Matsuo, Takashi Nakayama, Akihiko Ito, Hiroshi Munakata, Takao Satou
JournalJournal of neural transmission (Vienna, Austria : 1996) (J Neural Transm (Vienna)) Vol. 120 Issue 5 Pg. 767-83 (May 2013) ISSN: 1435-1463 [Electronic] Austria
PMID23180302 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Aldehydes
  • DNA, Single-Stranded
  • Glial Fibrillary Acidic Protein
  • Neuroprotective Agents
  • Proto-Oncogene Proteins c-bcl-2
  • 8-Hydroxy-2'-Deoxyguanosine
  • Catechin
  • epigallocatechin gallate
  • Phosphopyruvate Hydratase
  • Deoxyguanosine
  • 4-hydroxy-2-nonenal
Topics
  • 8-Hydroxy-2'-Deoxyguanosine
  • Aldehydes (metabolism)
  • Animals
  • Brain Edema (etiology, prevention & control)
  • Brain Injuries (complications, pathology, prevention & control)
  • Catechin (analogs & derivatives, therapeutic use)
  • DNA, Single-Stranded (metabolism)
  • Deoxyguanosine (analogs & derivatives, metabolism)
  • Disease Models, Animal
  • Drug Administration Schedule
  • Glial Fibrillary Acidic Protein (metabolism)
  • Lipid Peroxidation (drug effects)
  • Male
  • Maze Learning (drug effects)
  • Neurons (drug effects, metabolism)
  • Neuroprotective Agents (therapeutic use)
  • Phosphopyruvate Hydratase (metabolism)
  • Proto-Oncogene Proteins c-bcl-2 (metabolism)
  • Rats
  • Rats, Wistar
  • Time Factors

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