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作 者:单慧毓 张冬梅[1] 卢靖[1] 王健[1] SHAN Huiyu;ZHANG Dongmei;LU Jing;WANG Jian(Changchun University of Chinese Medicine,Changchun 130117,China)
机构地区:[1]长春中医药大学,长春130117
出 处:《吉林中医药》2020年第6期792-795,共4页Jilin Journal of Chinese Medicine
基 金:国家自然科学基金课题(81273687);国家中医药管理局课题(JDZX2015043);吉林省科技厅课题(20190905005SF)。
摘 要:目的讨论抵当汤对脑出血大鼠的内质网应激损伤而导致的神经细胞凋亡相关的信号蛋白真核细胞起始因子(eIF2α)、磷酸化真核细胞起始因子(p-eIF2α)及特异性蛋白C增强子结合蛋白同源蛋白(CHOP)表达的影响。方法以健康的Wistar大鼠60只作为研究对象,采用自体血注射尾状核的方法制作大鼠脑出血模型,将大鼠随机分为5组:假手术组、模型组,以及抵当汤低、中、高剂量组,每组 12只。采用免疫蛋白印记(western blot)方法,比较各组eIF2α、p-eIF2α及CHOP蛋白在脑出血半暗带区的动态表达;采用Longa五级评分法对几组大鼠进行神经功能评分;采用Billot公式计算法测定出脑出血半暗带的脑含水量。结果与模型组比较,抵当汤组p-eIF2α及CHOP蛋白表达降低;与模型组比较,抵当汤组大鼠神经功能评分较模型组低;与模型组比较,抵当汤组大鼠脑含水量较模型组低。结论抵当汤可以通过下调p-eIF2α及CHOP蛋白的表达,抑制与细胞凋亡相关的信号通路的活化,从而抑制过度的内质网应激损伤,对脑出血半暗带区的神经细胞有保护作用,从而减轻凋亡。Objective This article discusses the effects of Didang decoction on the expression of eIF2α,p-eIF2αand CHOP in neuronal apoptosis-related signaling induced by endoplasmic reticulum stress in rats with intracerebral hemorrhage.Methods 60 healthy Wistar rats were used as the study subjects.The rat model of cerebral hemorrhage was made by autologous injection of caudate nucleus.The rats were randomly divided into 5 groups:sham operation group,model group,and Didang decoctionlow,medium and high measurement groups,12 in each group.Western blot analysis was used to compare the dynamic expression of eIF2α,p-eIF2αand CHOP proteins of cerebral hemorrhage;Several groups of rats were scored for neurological function using the Longa five-level scoring method;Brain water content in the penumbra of the cerebral hemorrhage was determined by the calculation of the Billot formula.Results Compared with the model group,the expression of p-eIF2αand CHOP protein in the Didang decoctionwas reduced.Compared with the model group,the neurological function scores of the rats in the Didang decoctiongroup were lower than those in the model group.Compared with the model group,the brain water content of the DDT group was lower than that of the model group.Conclusion Didang decoctioncan inhibit the activation of signaling pathways related to apoptosis by down-regulating the expression of p-eIF2αand CHOP proteins,thereby inhibiting excessive endoplasmic reticulum stress injury,protects nerve cells in the penumbra of the cerebral hemorrhage,thereby attenuating apoptosis.
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