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Neuroprotection of ginsenoside Re in cerebral ischemia-reperfusion injury in rats.

机译:人参皂甙Re对大鼠脑缺血再灌注损伤的神经保护作用。

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摘要

In the present study, we have investigated the neuroprotective potential of ginsenoside Re (Re) in the middle cerebral artery occlusion model in Sprague-Dawley rats. Adult male Sprague-Dawley rats were treated with Re (5, 10 or 20 mg kg(- 1), P.O. for 7 days, once a day) prior to occlusion. There was a significant increase in the neurological symptoms in ischemic animals as compared with the sham group animals. These effects were attenuated by 10 and 20 mg kg(- 1) Re, P.O. There was a significant increase in the level of malondialdehyde (MDA) in ischemic animals indicating oxidative stress. An elevated level of MDA in ischemic animals was reduced by 10 and 20 mg kg(- 1) Re, P.O., respectively. It was observed that Re significantly decreased mitochondrial swelling, thereby preventing the reduction of H(+)-ATPase activity. This study demonstrates the neuroprotective potential of Re in cerebral ischemia-reperfusion injury in rats.
机译:在本研究中,我们研究了人参皂甙Re(Re)在Sprague-Dawley大鼠的大脑中动脉闭塞模型中的神经保护作用。成年雄性Sprague-Dawley大鼠在闭塞前接受Re(5、10或20 mg kg(-1),P.O。治疗7天,每天一次)。与假手术组动物相比,缺血动物的神经系统症状明显增加。这些作用减弱了10和20 mg kg(-1)Re,P.O.在缺血动物中,丙二醛(MDA)含量显着增加,表明存在氧化应激。缺血动物中MDA的升高水平分别降低了10和20 mg kg(-1)Re,P.O.。观察到Re明显降低了线粒体肿胀,从而防止了H(+)-ATPase活性的降低。这项研究证明了Re在大鼠脑缺血再灌注损伤中的神经保护作用。

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