Jt. Hong et al., Protective effect of green tea extract on ischemia/reperfusion-induced brain injury in Mongolian gerbils, BRAIN RES, 888(1), 2001, pp. 11-18
Free radical-induced oxidative damages of macromolecules and cell death are
important factors in the pathogenesis of ischemia/reperfusion brain injury
. In the present study, an investigation as to whether green tea extract re
duces ischemia/reperfusion-induced brain injury in Mongolian gerbils was co
nducted. The effect of green tea on the ischemia/reperfusion-induced produc
tion of hydrogen peroxide, lipid peroxidation and oxidative DNA damage (for
mation of 8-hydroxydeoxyguanosine), and cell death in addition to locomotor
activity was studied. Two doses (0.5 or 2%) of green tea extract were adde
d into the drinking water and to be accessed by animals ad libitum for 3 we
eks prior to the induction of ischemia. A global ischemia was induced by th
e bilateral occlusion of the common carotid arteries for 5 min. Reperfusion
was achieved by releasing the occlusion and restoring blood circulation fo
r 48 h. The infarction volumes were 112+/-31 mm(3) and 76+/-11 mm(3) in the
0.5 and 2% green tea pretreated animals compared to 189+/-12 mm(3) in the
ischemia/reperufusion animals. Green tea extract also reduced the levels of
ischemia/reperfusion-induced hydrogen peroxide (from 1470+/-170 to 1034+/-
46 and 555+/-30 nmole/mg protein), lipid peroxidation products (from 1410+/
-210 to 930+/-40 and 330+/-20 nmole/mg protein) and 8-oxodG (from 3.9+/-0.1
to 2.8+/-0.3 and 1.9+/-0.3 ng/mug DNA, X 10(-2)) by pretreatment of 0.5 or
2% green tea for 3 weeks, respectively. Moreover, green tea also reduced t
he number of ischemia/reperfusion-induced apoptotic cells (from 59+/-12 to
37+/-8. 15+/-11 apoptotic cells/high power field in the striatum region) an
d locomotor activity (from 15140+/-2940 to 3900+/-600 and 4100+/-1200). Thi
s study therefore suggests that green tea may be a useful agent for the pre
vention of cerebral ischemia damage. (C) 2001 Elsevier Science B.V. All rig
hts reserved.