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在脑缺血短暂模型中,外周给予甘草次酸可减轻缺血再灌注损伤。

Peripheral administration of carbenoxolone reduces ischemic reperfusion injury in transient model of cerebral ischemia.

作者信息

Vakili Abedin, Hosseinzadeh Seyed Ahmad, Khorasani Mahdi Zahedi

机构信息

Laboratory of Cerebrovascular Research, Department and Research Center of Physiology, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran.

出版信息

J Stroke Cerebrovasc Dis. 2009 Mar-Apr;18(2):81-5. doi: 10.1016/j.jstrokecerebrovasdis.2008.09.018.

Abstract

Carbenoxolone (CBX) has a neuroprotective effect in experimental models of brain ischemia and trauma. However, systemic effect of CBX on ischemic reperfusion injuries has not been investigated in a temporary model of focal cerebral ischemia. Male Wistar rats (n = 32) were divided into control and CBX-treated (100, 200, or 400 mg/kg, intraperitoneally) groups. Transient focal cerebral ischemia was induced by 60-minute middle cerebral artery occlusion by filament method, followed by 23-hour reperfusion. At the end of 24-hour ischemia, neurologic deficit score was tested and infarct volumes were determined using triphenyltetrazolium chloride staining. Administration of CBX (100, 200, or 400 mg/kg) at the beginning of ischemia significantly reduced cortical infarct volumes by 48%, 58%, and 63%, and striatal infarct volumes by 34%, 63%, and 63%, respectively. Nevertheless, CBX has no effect on neurologic dysfunction. Our findings indicated that peripheral administration of CBX has a neuroprotective effect on postischemic damage in a temporary model of focal cerebral ischemia in rat.

摘要

甘草次酸(CBX)在脑缺血和创伤的实验模型中具有神经保护作用。然而,在局灶性脑缺血的临时模型中,尚未研究CBX对缺血再灌注损伤的全身作用。将雄性Wistar大鼠(n = 32)分为对照组和CBX治疗组(腹腔注射100、200或400 mg/kg)。采用线栓法阻断大脑中动脉60分钟诱导短暂性局灶性脑缺血,随后进行23小时再灌注。在缺血24小时结束时,测试神经功能缺损评分,并使用氯化三苯基四氮唑染色法测定梗死体积。在缺血开始时给予CBX(100、200或400 mg/kg)可使皮质梗死体积分别显著减少48%、58%和63%,纹状体梗死体积分别显著减少34%、63%和63%。然而,CBX对神经功能障碍没有影响。我们的研究结果表明,在大鼠局灶性脑缺血的临时模型中,外周给予CBX对缺血后损伤具有神经保护作用。

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