摘要
目的 观察褪黑素 (MT)对脑缺血沙土鼠海马丙二醛 (MDA)含量和超氧化物歧化酶 (SOD)活性的影响 ,探讨其神经保护作用的机制。方法 采用沙土鼠双侧颈总动脉结扎法建立脑缺血再灌注模型 ,于缺血前 30min给予不同剂量的褪黑素 ,缺血 10min再灌注 1h后测定海马MDA含量和SOD活性。结果 脑缺血再灌注 1h后海马MDA含量升高 ,而SOD活性降低 ,给予MT可部分逆转这种改变。结论 MT能够降低脑缺血再灌注沙土鼠海马的MDA含量 。
Objective To probe into the mechanism of the neuroprotective effect of melatonin (MT) by investigating its effects on malondialdehyde (MDA) contents and superoxide dismutase (SOD) activities in the hippocampus of gerbils after cerebral ischemia-reperfusion.?Methods Occlusion of bilateral carotid arteries was adopted to prepare gerbil cerebral ischemia-reperfusion models. Different doses of MT were administered ip 30 min prior to the occlusion. After 10 min of ischemia and 1 h of reperfusion, bilateral hippocampi were removed for the study of MDA and SOD.?Results The contents of MDA were markedly elevated and the SOD activities decreased in the hippocampus 1 h after reperfusion. MT could partly reverse the elevation of MDA content and the reduction of SOD activity.?Conclusion MT can reduce the lipid peroxidation by keeping up the activity of SOD in ischemia-reperfusion gerbils, exerting its neuroprotective effect.
出处
《徐州医学院学报》
CAS
2001年第4期324-326,共3页
Acta Academiae Medicinae Xuzhou
关键词
褪黑素
脑缺血再灌注损伤
丙二醛
超氧化物歧化酶
脂质过氧化
沙土鼠
melatonin
gerbil
cerebral ischemia-reperfusion injury
malondialdehyde
superoxide dismutase
lipid peroxidation
