Neuroprotective effect of green tea extract in experimental ischemia-reperfusion brain injury
Author: Jin Tae Hong and Seung Rel Ryu and Hye Jin Kim and Jong Kwon Lee and Sun Hee Lee and Dai Byung Kim and Yeo Pyo Yun and Jong Hoon Ryu and Byung Mu Lee and Pu Young Kim
Eicosanoids accumulation and formation of oxygen free radicals have been implicated in the pathogenesis of ischemia/reperfusion brain injury. In the present study, we examined whether green tea extract protects against ischemia/reperfusion-induced brain injury by minimizing eicosanoid accumulation and 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 arteries for 60 min and reperfusion was achieved for 24 h. Infarction volume in the ipsilateral hemisphere of ischemia/reperfusion animals was 114 ± 16 mm3 in the 0.5% green tea pretreated animals compared to 180 ± 54 mm3 in left hemisphere of nontreated animals. Green tea extract (0.5%) also reduced ischemia/reperfusion-induced eicosanoid concentration: Leukotriene C4 (from 245 ± 51 to186 ± 22), prostoglandin E2 (from 306 ± 71 to 212 ± 43) and thromboxane A2 (327 ± 69 to 251 ± 87 ng/mg protein). Ischemia/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/μg DNA, ×10−2) were also reduced. Moreover, 0.5% green tea extract also reduced the apoptotic cell number (from 44 ± 11 to 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 active avoidance. The present study shows that the minimizing effect of green tea extract on the eicosanoid accumulation and oxidative damage in addition to the reduction of neuronal cell death could eventually result in protective effect on the ischemia/reperfusion-induced brain injury and behavior deficit.
