[논문]Neuroprotective effect of green tea extract in experimental ischemia-reperfusion brain injury

doi:10.1016/S0361-9230(00)00348-8

[해외논문] Neuroprotective effect of green tea extract in experimental ischemia-reperfusion brain injury

Brain research bulletin, v.53 no.6, 2000년, pp.743 - 749

Hong, Jin Tae (National Institute of Toxicological Research, Korea Food and Drug Administration, Seoul, South Korea) , Ryu, Seung Rel (National Institute of Toxicological Research, Korea Food and Drug Administration, Seoul, South Korea) , Kim, Hye Jin (National Institute of Toxicological Research, Korea Food and Drug Administration, Seoul, South Korea) , Lee, Jong Kwon (National Institute of Toxicological Research, Korea Food and Drug Administration, Seoul, South Korea) , Lee, Sun Hee (National Institute of Toxicological Research, Korea Food and Drug Administration, Seoul, South Korea) , Kim, Dai Byung (National Institute of Toxicological Research, Korea Food and Drug Administration, Seoul, South Korea) , Yun, Yeo Pyo (College of Pharmacy, Chungbuk National University, Chungbuk, South Korea) , Ryu, Jong Hoon (College of Pharmacy, Kyung Hee University, Seoul, South Korea) , Lee, Byung Mu (Division of Toxicology, College of Pharmacy, SengKyunKwan University, Kyunggido, South Korea) , Kim, Pu Young (National Institute of Toxicological Research, Korea Food and Drug Administration, Seoul, South Korea)

Abstract ▼ AI-Helper

AbstractEicosanoids 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.

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