NeuroMolecular Medicine

, Volume 13, Issue 4, pp 300–309 | Cite as

(−)-Epigallocatechin-3-gallate Protects Against Neuronal Cell Death and Improves Cerebral Function After Traumatic Brain Injury in Rats

  • Tatsuki ItohEmail author
  • Motohiro Imano
  • Shozo Nishida
  • Masahiro Tsubaki
  • Shigeo Hashimoto
  • Akihiko Ito
  • Takao Satou
Original Paper


A major component of green tea, a widely consumed beverage, is (−)-epigallocatechin gallate (EGCG), which has strong antioxidant properties. Our previous study has indicated that free radical production following rat traumatic brain injury (TBI) induces neural degeneration. In this study, we investigated the effects of EGCG on cerebral function and morphology following TBI. Six-week-old male Wistar rats that had access to normal drinking water, or water containing 0.1% (w/v) EGCG ad libitum, received TBI 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 the levels of malondialdehyde (MDA) around the damaged area after TBI, significantly decreased in the EGCG treatment group compared with the water group (P < 0.05). Most ssDNA-positive cells in the water group co-localized with neuronal cells. However, in the EGCG treatment group, few ssDNA-positive cells co-localized with neurons. In addition, there was a significant increase in the number of surviving neuronal cells and an improvement in cerebral dysfunction after TBI in the EGCG treatment group compared with the water group (P < 0.05). These results indicate that consumption of water containing EGCG pre- and post-TBI inhibits free radical–induced neuronal degeneration and apoptotic cell death around the damaged area, resulting in the improvement of cerebral function following TBI. In summary, consumption of green tea may be an effective therapy for TBI patients.


Epigallocatechin Traumatic brain injury Neuroprotection Apoptosis Oxidative stress 



This work was supported by the Grant-in-Aid for Scientific Research (21500803). The authors thank Mari Yachi for technical assistance.

Conflict of interest

The authors declare they have no conflict of interest.


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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Tatsuki Itoh
    • 1
    Email author
  • Motohiro Imano
    • 2
  • Shozo Nishida
    • 3
  • Masahiro Tsubaki
    • 3
  • Shigeo Hashimoto
    • 4
  • Akihiko Ito
    • 1
  • Takao Satou
    • 1
    • 5
    • 6
  1. 1.Department of Pathology, Faculty of MedicineKinki UniversityOsakaJapan
  2. 2.Department of Surgery, Faculty of MedicineKinki UniversityOsakaJapan
  3. 3.Faculty of Pharmaceutical SciencesKinki UniversityOsakaJapan
  4. 4.Department of PathologyPL HospitalOsakaJapan
  5. 5.Division of Sports Medicine, Institute of Life ScienceKinki UniversityOsakaJapan
  6. 6.Division of Hospital Pathology, Faculty of MedicineHospital of Kinki UniversityOsakaJapan

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