Hong J T, Ryu S R, Kim H J, Lee J K, Lee S H, Yun Y P, Lee B M, Kim P Y
National Institute of Toxicological Research, Korea Food and Drug Administration, 5, Nokbun-dong, Eunpyung-gu, 122-704, Seoul, South Korea.
Brain Res. 2001 Jan 5;888(1):11-18. doi: 10.1016/s0006-8993(00)02935-8.
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.
自由基诱导的大分子氧化损伤和细胞死亡是缺血/再灌注脑损伤发病机制中的重要因素。在本研究中,我们对绿茶提取物是否能减轻沙土鼠缺血/再灌注诱导的脑损伤进行了调查。研究了绿茶对缺血/再灌注诱导的过氧化氢产生、脂质过氧化和氧化性DNA损伤(8-羟基脱氧鸟苷的形成)以及细胞死亡和运动活性的影响。在诱导缺血前3周,将两种剂量(0.5%或2%)的绿茶提取物添加到饮用水中,供动物随意饮用。通过双侧颈总动脉闭塞5分钟诱导全脑缺血。通过解除闭塞并恢复血液循环48小时实现再灌注。与缺血/再灌注动物的189±12mm³相比,0.5%和2%绿茶预处理动物的梗死体积分别为112±31mm³和76±11mm³。绿茶提取物还通过分别用0.5%或2%绿茶预处理3周,降低了缺血/再灌注诱导的过氧化氢水平(从1470±170降至1034±46和555±30nmol/mg蛋白)、脂质过氧化产物水平(从1410±210降至930±40和330±20nmol/mg蛋白)和8-氧代脱氧鸟苷水平(从3.9±0.1降至2.8±0.3和1.9±0.3ng/μg DNA,×10⁻²)。此外,绿茶还减少了缺血/再灌注诱导的凋亡细胞数量(从59±12降至37±8,纹状体区域每高倍视野15±11个凋亡细胞)和运动活性(从15140±2940降至3900±600和4100±1200)。因此,本研究表明绿茶可能是预防脑缺血损伤的有用药物。