Protection of active oxygen-related neuronal injuries by tea catechins

The activities of tea catechins, (+)-catechin (CA), (-)-epicatechin (EC) and (-)-epigallocatechin gallate (EGg), on scavenging 1,1-diphenyl-2-picrylhydrazyl radical, superoxide anion radical and hydroxyl radical were examined by using colorimeter, chemiluminescence reader and ESR spectrometer, and t...

Full description

Saved in:
Bibliographic Details
Published inJapanese Journal of Pharmacology Vol. 71; no. suppl.1; p. 102
Main Authors Annaka, Toshimitsu, Kobori, Yoshiko, Matsuoka, Yutaka, Sunagane, Nobuyoshi, Uruno, Tsutomu, Kubota, Kazuhiko
Format Journal Article
LanguageEnglish
Japanese
Published The Japanese Pharmacological Society 1996
Online AccessGet full text

Cover

Loading…
More Information
Summary:The activities of tea catechins, (+)-catechin (CA), (-)-epicatechin (EC) and (-)-epigallocatechin gallate (EGg), on scavenging 1,1-diphenyl-2-picrylhydrazyl radical, superoxide anion radical and hydroxyl radical were examined by using colorimeter, chemiluminescence reader and ESR spectrometer, and the order of the scavenging activity was EGg>>EC≒CA. In order to examine the effects of tea catechins on the protection of neuronal injury by active oxygens, cultured newborn-mouse cerebral neurons were injured by hypoxanthine/xanthine oxidase (HPX/XOD) or glucose oxidase (GOD). EGg was strongest in the protection of the cell injury by HPX/XOD, but weakest in that by GOD. The memory impairment of mice was produced by 10 min occlusion of the bilateral common carotid arteries. Learning ability of mice was assessed by a step-down-type passive avoidance test. The i.v. injection of CA or EC ameliorated the memory impairment, but EGg did not. These results suggests that the in vivo activity of tea catechins on the protection against active oxygen injury greatly dependent on their permeability to cell membrane. Tea catechins like EC and CA that can scavenge intra- and extra-cellular active oxygen species may be useful in ameliorating the various diseases induced by active oxygens.
ISSN:0021-5198
DOI:10.1016/S0021-5198(19)36646-6