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作 者:梁华峰[1] 王娟[1] 谢靖[1] 余鹃 申婧[1] 田凤[1] 刘春红[1] 张惠丽[1]
机构地区:[1]新疆石河子大学医学院第一附属医院神经内科,新疆石河子832000
出 处:《中国病理生理杂志》2017年第10期1768-1772,共5页Chinese Journal of Pathophysiology
基 金:兵团应用基础研究计划(No.2015AG014)
摘 要:目的:观察盐酸水苏碱对实验性急性脑梗死大鼠的治疗效果,并探讨其可能作用机制。方法:将75只大鼠随机分为5组:假手术组、脑梗死组及不同剂量盐酸水苏碱治疗组,每组各15只。盐酸水苏碱治疗组大鼠在造模完成后分别给予盐酸水苏碱10 mg/kg、20 mg/kg和40 mg/kg灌胃,每天1次,连续给药14 d。给药完成后,对各组大鼠进行神经功能缺损评分,计算脑梗塞体积,干湿重法检测脑含水量,Western blot法检测脑组织中β-catenin、cyclin D1、糖原合成酶激酶3β(GSK-3β)和p-GSK-3β的蛋白水平。结果:与脑梗死组相比,盐酸水苏碱治疗后大鼠的神经功能缺损评分明显降低,脑梗死体积与脑含水量明显降低,β-catenin、cyclin D1和p-GSK-3β的蛋白水平明显升高。结论:盐酸水苏碱对实验性大鼠急性脑梗死具有一定的疗效,其机制可能与激活了Wnt/β-catenin信号通路有关。AIM:To observe the therapeutic effect of stachydrine hydrochloride on experimental acute cerebral infarction in rats and to explore the underlying mechanisms .METHODS:SD rats ( n=75) were randomly divided into 5 groups:sham group, cerebral infarction model group , and stachydrine hydrochloride (10 mg/kg, 20 mg/kg and 40 mg/kg) treatment groups .After the establishment of cerebral infarction model , the rats were given stachydrine hydrochloride at dose of 10 mg/kg, 20 mg/kg or 40 mg/kg by gavage daily for 14 d.The impairment of neurological function in each group was scored .The cerebral infarction volume and brain water content were measured .Moreover , the protein levels of β-cate-nin, cyclin D1, glycogen synthase kinase 3β(GSK-3β) and p-GSK-3βin the brain tissues were detected by Western blot . RESULTS:Compared with cerebral infarction group , the score of neurological function impairment , cerebral infarction volume and brain water content were significantly decreased in stachydrine hydrochloride treatment groups .In addition , the protein levels of β-catenin, cyclin D1 and p-GSK-3βwere markedly increased after stachydrine hydrochloride treatment . CONCLUSION:Stachydrine hydrochloride protects against experimental acute cerebral infarction through activation of Wnt/β-catenin signaling pathway .
关 键 词:盐酸水苏碱 急性脑梗死 WNT/Β-CATENIN信号通路
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