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白杨素可减轻大鼠短暂局灶性缺血后的脑梗死。

Apocynin attenuates cerebral infarction after transient focal ischaemia in rats.

作者信息

Tang L L, Ye K, Yang X F, Zheng J S

机构信息

Department of Infectious Disease, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, The People's Republic of China.

出版信息

J Int Med Res. 2007 Jul-Aug;35(4):517-22. doi: 10.1177/147323000703500411.

Abstract

This study investigated whether inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase attenuates cerebral infarction after transient focal ischaemia in rats. Focal ischaemia (1.5 h) was produced in male Sprague-Dawley rats (250 - 280 g) by middle cerebral artery occlusion. Some rats also received treatment with 50 mg/kg apocynin, a NADPH oxidase inhibitor, by intraperitoneal injection 30 min prior to reperfusion. Two hours after reperfusion, brains were harvested to measure NADPH oxidase activity and superoxide levels. After 24 h, the remaining brains were harvested to investigate infarct size. NADPH oxidase activity and superoxide level were all augmented 2 h after reperfusion compared with controls. Apocynin treatment significantly reduced NADPH oxidase activity and superoxide levels. Cerebral infarct size was significantly smaller in the apocynin-treated group compared with those undergoing ischaemia/reperfusion alone. These results indicate that inhibition of NADPH oxidase attenuates cerebral infarction after transient focal ischaemia in rats, suggesting that inhibition of NADPH oxidase may provide a therapeutic strategy for ischaemic stroke.

摘要

本研究调查了抑制还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶是否能减轻大鼠短暂性局灶性缺血后的脑梗死。通过大脑中动脉闭塞在雄性Sprague-Dawley大鼠(250 - 280 g)中产生局灶性缺血(1.5小时)。一些大鼠在再灌注前30分钟还通过腹腔注射接受了50 mg/kg的Apocynin(一种NADPH氧化酶抑制剂)治疗。再灌注2小时后,收获大脑以测量NADPH氧化酶活性和超氧化物水平。24小时后,收获剩余大脑以研究梗死面积。与对照组相比,再灌注2小时后NADPH氧化酶活性和超氧化物水平均升高。Apocynin治疗显著降低了NADPH氧化酶活性和超氧化物水平。与单独进行缺血/再灌注的大鼠相比,Apocynin治疗组的脑梗死面积明显更小。这些结果表明,抑制NADPH氧化酶可减轻大鼠短暂性局灶性缺血后的脑梗死,提示抑制NADPH氧化酶可能为缺血性中风提供一种治疗策略。

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