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目的研究和厚朴酚对局灶性脑缺血的保护作用和缺血再灌注脑组织对活性氧清除能力的影响。方法用线栓法造成大鼠大脑中动脉阻塞模型,观察大鼠行为学改变和脑梗死体积。用双侧颈动脉结扎30 min,再灌注30 min造成小鼠脑缺血再灌注损伤,测定脑组织中相关酶的活性,脂质过氧化产物丙二醛的含量和脑组织Na+-K+-ATP酶的活性。结果和厚朴酚5 ~50μg·kg-1在大脑中动脉阻塞后0.25和3 h iv给药,可显著改善脑缺血大鼠的神经学评分,明显减少脑梗死体积。和厚朴酚7 ~70μg·kg-1分别于阻塞前和再灌注前2 min iv给药,可明显升高小鼠脑组织中超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和过氧化物酶的活性;显著降低丙二醛的含量。同时和厚朴酚也升高脑组织Na+-K+-ATP酶的活性。结论和厚朴酚可改善局部脑缺血引起的神经行为缺陷和缩小脑梗死体积;并提高缺血再灌注脑组织对活性氧的清除能力和Na+-K+-ATP酶活性,表明它对脑缺血和缺血再灌注损伤均有保护作用。
Objective To investigate the protective effect of honokiol on focal cerebral ischemia and the effect of holoprostol on the scavenging capacity of reactive oxygen species. Methods The model of middle cerebral artery occlusion in rats was established by suture method. The behavioral changes and cerebral infarct volume were observed. Cerebral ischemia-reperfusion injury was induced by bilateral carotid artery ligation for 30 min and reperfusion for 30 min. The activity of related enzymes in brain tissue was measured. The content of lipid peroxidation product malondialdehyde and brain tissue Na+-K+-ATP were measured. Enzyme activity. Results The administration of honokiol at a dose of 5 to 50 μg·kg-1 for 0.25 and 3 h after middle cerebral artery occlusion can significantly improve the neurological scores of cerebral ischemic rats and significantly reduce the infarct volume. Administration of honokiol at 7-70 μg·kg-1 to iv before and 2 min before reperfusion could significantly increase the superoxide dismutase, catalase and glutathione peroxidation in mouse brain tissue. Enzymatic and peroxidase activity; significantly reduced malondialdehyde content. At the same time, honokiol also increased the activity of Na+-K+-ATPase in brain tissue. Conclusion Honokiol can improve the neurobehavioral deficits caused by focal cerebral ischemia and reduce the volume of cerebral infarction; and increase the scavenging capacity of active oxygen and Na+-K+-ATPase activity in brain tissue after ischemia-reperfusion, which indicates that it has a brain deficiency. Blood and ischemia reperfusion injury have protective effects.