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57. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie (DGNN)

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie

12. - 15.09.2012, Erlangen

Banner: 57. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie

Protective effects of epigallocatechin-3-gallate against hippocampal neuronal damage in pentylenetetrazole-induced seizures in rats

Meeting Abstract

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  • presenting/speaker weiping wang - neurology deparment, shijiazhuang, China
  • tao xie - neurology deparment, shijiazhuang, China

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Erlangen, 12.-15.09.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12dgnnPP6.5

DOI: 10.3205/12dgnn116, URN: urn:nbn:de:0183-12dgnn1162

Veröffentlicht: 11. September 2012

© 2012 wang et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Question: Temporal lobe epilepsy is most commonly associated with hippocampus neurons loss. Epigallocatechin gallate (EGCG) is a major compound of green tea polyphenol that has been revealed the neuroprotective effects in a variety of neural injury. Thus the purpose of this study was to evaluate whether EGCG could reduce neuronal damage in pentylenetetrazol (PTZ) induced seizures and explore the possible underling mechanisms.

Methods: Male Sprague-Dawley rats were devided into 4 groups. Group 1 was injected with saline. Group 2 was injected with a dose of 35 mg/kg of PTZ once alternate day for 13 injections. In group3 and group 4, EGCG was administered daily in two doses (25 mg/kg and 50 mg/kg) intraperitoneally along with alternate-day PTZ. The rats were sacrificed twenty-four hours after the last administration. Neuronal cell damage in the hippocampal CA1 and CA3 region was evaluated by Nissl staining. The expression of caspase-3, Bcl-2, Bax, p-PI3K and p-Akt were detected by western blots.

Results: The results showed that EGCG significantly attenuated the neuronal loss in a dose-dependent manner. EGCG significantly elevated p-PI3K and p-Akt protein level, markedly increased Bcl-2 expression, decreased Bax and caspase-3 protein level compared to the kindled rats.

Conclusions: These observations indicate that EGCG could attenuate PTZ-induced hippocampal neuronal damage and the underlying mechanisms might be related to the regulation of the PI3K/Akt signaling pathway and the inhibition of the mitochondrial apoptosis pathway. Therefore, EGCG might be a protective agent against hippocampal neuronal damage in PTZ-induced seizures.