Eicosanoids accumulation and formation of oxygen free radicals have been im
plicated in the pathogenesis of ischemia/reperfusion brain injury. In the p
resent study, we examined whether green tea extract protects against ischem
ia/reperfusion-induced brain injury by minimizing eicosanoid accumulation a
nd oxygen radical-induced oxidative damage in the brain. Green tea extract
(0.5%) was orally administered to Wistar rats for 3 weeks before induction
of ischemia, Ischemia was induced by the occlusion of middle cerebral arter
ies for 60 min and reperfusion was achieved for 24 h. Infarction volume in
the ipsilateral hemisphere of ischemia/reperfusion animals was 114 +/- 16 m
m(3) in the 0.5% green tea pretreated animals compared to 180 +/- 54 mm(3)
in left hemisphere of nontreated animals, Green tea extract (0.5%) also red
uced ischemia/reperfusion-induced eicosanoid concentration: Leukotriene C-4
(from 245 +/- 51 to186 +/- 22), prostoglandin E-2 (from 306 +/- 71 to 212
+/- 43) and thromboxane A(2) (327 +/- 69 to 251 +/- 87 ng/mg protein). Isch
emia/reperfusion-induced increases of hydrogen peroxide level (from 688 +/-
76 to 501 +/- 99 nmole/mg protein), lipid peroxidation products (from 1010
+/- 110 to 820 +/- 70 nmole/mg protein) and 8-oxodG formation (from 1.3 +/
- 0.3 to 0.8 +/- 0.2 ng/mug DNA, x10(-2)) were also reduced. Moreover, 0.5%
green tea extract also reduced the apoptotic cell number (from 44 +/- 11 t
o 29 +/- 1 in the striatum, and from 72 +/- 11 to 42 +/- 5 apoptotic cells/
high power field in the cortex region). Green tea extract pretreatment also
promoted recovery from the ischemia/reperfusion-induced inhibition of acti
ve avoidance, The present study shows that the minimizing effect of green t
ea extract on the eicosanoid accumulation and oxidative damage in addition
to the reduction of neuronal cell death could eventually result in protecti
ve effect on the ischemia/reperfusion-induced brain injury and behavior def
icit. (C) 2001 Elsevier Science Inc.