title: Protective effect of green tea extract on ischemia/reperfusion-induced brain injury in Mongolian gerbils.
abstract: 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 reduces ischemia/reperfusion-induced brain injury in Mongolian gerbils was conducted. The effect of green tea on the ischemia/reperfusion-induced production of hydrogen peroxide, lipid peroxidation and oxidative DNA damage (formation of 8-hydroxydeoxyguanosine), and cell death in addition to locomotor activity was studied. Two doses (0.5 or 2%) of green tea extract were added into the drinking water and to be accessed by animals ad libitum for 3 weeks prior to the induction of ischemia. A global ischemia was induced by the bilateral occlusion of the common carotid arteries for 5 min. Reperfusion was achieved by releasing the occlusion and restoring blood circulation for 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/reperfusion 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 and1.9+/-0.3 ng/microg DNA, x10(-2)) by pretreatment of 0.5 or 2% green tea for 3 weeks, respectively. Moreover, green tea also reduced the number of ischemia/reperfusion-induced apoptotic cells (from 59+/-12 to 37+/-8, 15+/-11 apoptotic cells/high power field in the striatum region) and locomotor activity (from 15140+/-2940 to 3900+/-600 and 4100+/-1200). This study therefore suggests that green tea may be a useful agent for the prevention of cerebral ischemia damage.
authors.affiliation: National Institute of Toxicological Research, Korea Food and Drug Administration, 5, Nokbun-dong, Eunpyung-gu, 122-704, Seoul, South Korea. jinthong@kfda.go.kr
authors.forename: J T
authors.initials: JT
authors.lastname: Hong
authors.forename: S R
authors.initials: SR
authors.lastname: Ryu
authors.forename: H J
authors.initials: HJ
authors.lastname: Kim
authors.forename: J K
authors.initials: JK
authors.lastname: Lee
authors.forename: S H
authors.initials: SH
authors.lastname: Lee
authors.forename: Y P
authors.initials: YP
authors.lastname: Yun
authors.forename: B M
authors.initials: BM
authors.lastname: Lee
authors.forename: P Y
authors.initials: PY
authors.lastname: Kim
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001628:Beverages; D001921:Brain / Q000098:blood supply / Q000166:cytology / Q000378:metabolism*; D020520:Brain Infarction / Q000188:drug therapy; D002560:Cerebrovascular Circulation / Q000187:drug effects; D015853:Cysteine Proteinase Inhibitors / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D003849:Deoxyguanosine / Q000031:analogs & derivatives* / Q000378:metabolism; D005260:Female; D005849:Gerbillinae; D006861:Hydrogen Peroxide / Q000378:metabolism; D002546:Ischemic Attack, Transient / Q000188:drug therapy*; D015227:Lipid Peroxidation / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D009043:Motor Activity / Q000187:drug effects; D009474:Neurons / Q000166:cytology / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D010936:Plant Extracts / Q000494:pharmacology*; D015427:Reperfusion Injury / Q000188:drug therapy*
chemical_list: D000447:Aldehydes; D015853:Cysteine Proteinase Inhibitors; D010936:Plant Extracts; D008315:Malondialdehyde; D000080242:8-Hydroxy-2'-Deoxyguanosine; D004247:DNA; D006861:Hydrogen Peroxide; D003849:Deoxyguanosine; C027576:4-hydroxy-2-nonenal