Protective effects of green tea catechins on cerebral ischemic damage.
BACKGROUND
Green tea catechins possess potent antioxidative properties, and the preventive effects against various oxidative diseases have been reported. The purpose of this study is to examine preventive and protective effects of green tea catechins on various deteriorative processes following stroke.


METHODS
Male Wistar rats were given ad libitum water with or without 0.25 and 0.5% tea catechin extract for 5 days prior to the operation and during the experiment. Right middle cerebral artery was occluded for 2 h, then reperfused for 22 h. Brain slices were stained with triphenyltetrazolim chloride to assess infarct area. Concentrations of plasma EGCg, and serum NOx were analyzed by HPLC. Detection of iNOS expression, neutrophil infiltration and peroxynitrite formation in the penumbra was performed by immunostain. Neurologic deficit was scored by posture reflex.


RESULTS
Tea catechins dose-dependently reduced the brain infarct area and volume. Infarct volume was inversely correlated with plasma EGCg concentration. Dark staining for iNOS, neutrophils and peroxynitrite were observed in vessel wall of small arteries in control ischemic hemisphere, while in catechins (0.5%)-treated rats iNOS was detected slightly, and staining for neutrophils and peroxynitrite was not seen. Catechin ingestion blocked a 3-fold increase in serum NOx concentration in the jugular vein, and also reduced by 35% a 2-fold increase of plasma lipid peroxide level seen in control rats after reperfusion. Neurologic deficits were significantly alleviated by 0.5% catechin ingestion.


CONCLUSIONS
Daily intake of green tea catechins efficiently protects the penumbra from irreversible damage due to cerebral ischemia, and consequent neurologic deficits.
Suzuki
Motohisa
M
University of Shizuoka, Graduate School of Health Sciences, 52-1 Yada, Shizuoka 422-8526, Japan.
Tabuchi
Masaki
M
Ikeda
Masahiko
M
Umegaki
Keizo
K
Tomita
Takako
T
D000818:Animals; D002545:Brain Ischemia / Q000473:pathology / Q000517:prevention & control*; D002392:Catechin / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000097:blood / Q000494:pharmacology*; D002851:Chromatography, High Pressure Liquid; D004305:Dose-Response Relationship, Drug; D016179:Granulocyte Colony-Stimulating Factor; D016298:Hematopoietic Cell Growth Factors / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery; D007377:Interleukin-3; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009566:Nitrates / Q000097:blood; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D009573:Nitrites / Q000097:blood; D010936:Plant Extracts / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D011994:Recombinant Proteins; D013662:Tea; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000378:metabolism
D016298:Hematopoietic Cell Growth Factors; D007377:Interleukin-3; D009566:Nitrates; D009573:Nitrites; D010936:Plant Extracts; D011993:Recombinant Fusion Proteins; D011994:Recombinant Proteins; D013662:Tea; C404145:myelopoietin; D016179:Granulocyte Colony-Stimulating Factor; C002744:3-nitrotyrosine; D014443:Tyrosine; D008315:Malondialdehyde; D002392:Catechin; C045651:epigallocatechin gallate; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat