Protective effect of green tea extract on ischemia/reperfusion-induced brain injury in Mongolian gerbils

Protective effect of green tea extract on ischemia/reperfusion-induced brain injury in Mongolian... 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/μg DNA, ×10 −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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Elsevier

Protective effect of green tea extract on ischemia/reperfusion-induced brain injury in Mongolian gerbils

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Publisher
Elsevier
Copyright
Copyright © 2001 Elsevier Science B.V.
ISSN
0006-8993
DOI
10.1016/S0006-8993(00)02935-8
Publisher site
See Article on Publisher Site

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/μg DNA, ×10 −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.

Journal

Brain ResearchElsevier

Published: Jan 5, 2001

References

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