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作 者:王稳平 赵晓娟[2] WANG Wenping;ZHAO Xiaojuan(Internal Medicine Department,Weinan Traditional Chinese Medicine Hospital,Weinan 714000,China;College of Nursing,Weinan Vocational and Technical College,Weinan 714000,China)
机构地区:[1]渭南市中医医院内科,渭南714000 [2]渭南职业技术学院护理学院,渭南714000
出 处:《世界中医药》2022年第22期3158-3161,共4页World Chinese Medicine
基 金:陕西省科技计划项目(2016KJXX-56)。
摘 要:目的:研究补阳还五汤对急性大脑缺血再灌注损伤大鼠的作用及机制。方法:将30只无特定病原体(SPF)级SD大鼠随机分为假手术组、模型组、干预组,每组10只。模型组和干预组建立大脑缺血再灌注模型,干预组在造模前给予补阳还五汤灌胃,连续14 d,假手术组仅进行假手术操作。评价神经行为学评分、测定脑组织含水量及基因的mRNA表达量。结果:与假手术组比较,模型组大鼠的神经行为学评分明显升高、脑组织含水量明显增多,脑组织中BCL-2-相关X蛋白(Bax)、胱天蛋白酶-3的mRNA表达水平均明显上调,B细胞淋巴瘤-2(Bcl-2)、磷脂酰肌醇3激酶、蛋白激酶B的mRNA表达水平均明显下调;与模型组大鼠比较,干预组大鼠的神经行为学评分明显降低、脑组织含水量明显减少,脑组织中Bax、胱天蛋白酶-3的mRNA表达水平均明显下调,Bcl-2、磷脂酰肌醇3激酶、蛋白激酶B的mRNA表达水平均明显上调。结论:补阳还五汤能够减轻急性大脑缺血再灌注损伤,其机制可能与PI3K/AKT信号通路介导的凋亡抑制作用有关。Objective:To study the effect and mechanism of Buyang Huanwu Decoction on acute cerebral ischemia-reperfusion injury(CIRI)in rats.Methods:Thirty SD rats of SPF grade were randomly divided into a sham operation group,a model group,and a treatment group,with 10 rats in each group.The CIRI model was induced in rats of the model group and the treatment group.The rats in the treatment group received Buyang Huanwu Decoction by gavage for 14 consecutive days before modeling,and those in the sham operation group only underwent sham operation.The neurobehavioral score was evaluated,and water content in the brain and gene expression were measured.Results:Compared with the sham operation group,the model group showed increased neurobehavioral score,elevated water content in brain tissues,up-regulated mRNA expression levels of Bax and Caspase-3 in brain tissues,and down-regulated mRNA expression levels of Bcl-2,PI3K,and AKT.Compared with the model group,the treatment group showed decreased neurobehavioral score,reduced water content in brain tissues,down-regulated mRNA expression levels of Bax and Caspase-3 in brain tissues,and up-regulated expression levels of Bcl-2,PI3K,and AKT.Conclusion:Buyang Huanwu Decoction can alleviate acute CIRI,and its mechanism may be related to the inhibition of apoptosis mediated by the PI3K/AKT pathway.
关 键 词:大脑缺血再灌注 补阳还五汤 磷脂酰肌醇3激酶 蛋白激酶B 信号通路 凋亡 机制
分 类 号:R255.2[医药卫生—中医内科学]
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