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作 者:蒋希成[1] 段芳芳 张婷婷 孙晓伟[2] 姜国华 王兵[1] 张浩[2] 孙远征[3] 姜德友[1] JIANG Xicheng;DUAN Fangfang;ZHANG Tingting;SUN Xiaowei;JIANG Guohua;WANG Bing;ZHANG Hao;SUN Yuanzheng;JIANG Deyou(Heilongjiang University of Chinese Medicine,Harbin 150040,China;The First Affiliated Hospital of Heilongjiang University of Chinese Medicine,Harbin 150040,China;The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine,Harbin 150001,China)
机构地区:[1]黑龙江中医药大学,黑龙江哈尔滨150040 [2]黑龙江中医药大学附属第一医院,黑龙江哈尔滨150040 [3]黑龙江中医药大学附属第二医院,黑龙江哈尔滨150001
出 处:《中医药学报》2020年第12期21-25,共5页Acta Chinese Medicine and Pharmacology
基 金:国家自然科学基金面上项目(81673865,81503669);黑龙江省自然科学基金面上项目(H201327)。
摘 要:目的:通过PI3K-Akt-mTOR信号通路相关分子的研究,进一步探索芪蛭胶囊对脑缺血再灌注损伤(CIRI)的拮抗机理。方法:60只SD大鼠随机平均分成6组,sham组、模型组、3-MA组、雷帕霉素组、LY294002组和中药(芪蛭胶囊)组。MCAO模型复制前进行相应抑制剂及中药干预,再灌注24 h后进行NSS大鼠神经功能评分、TTC检测脑梗死体积、Western blot法检测脑组织PI3K、p-PI3K、Beclin-1蛋白表达,并分析其差异。结果:与模型组对比,中药组CIRI大鼠NSS神经功能评分显著降低,脑梗死体积显著缩小,脑组织p-PI3K水平下降,Beclin-1含量增加。结论:芪蛭胶囊能降低CIRI后NSS评分,减轻脑组织损伤,通过抑制PI3K的活化,上调Beclin-1蛋白的表达,进一步激活自噬,从而发挥拮抗CI/RI的作用。Objective:To explore the mechanism of Qizhi Capsule’s antagonism against cerebral ischemia reperfusion injury(CIRI)through the study on the related molecules of PI3 K-Akt-mTOR signaling pathway.Methods:60 SD rats were randomly divided into the sham group,the model group,3-MA group,Rapamycin group,LY294002 group and TCM group(Qizhi Capsule).The corresponding inhibitor and TCM medication were used before MCAO model replication.After that,Neurological Severity Scale(NSS)score was used to assess neurological function,TTC staining was used to detect cerebral infarction area,and Western blot was used to detect the protein expressions of PI3 K,p-PI3 k and Beclin-1 in brain tissue.Results:Compared to those in the model group,the NSS score of CIRI rats was significantly reduced,the volume of cerebral infarction was significantly decreased,the level of p-PI3 K in brain tissue was decreased,and the content of Beclin-1 was increased in TCM group.Conclusion:Qizhi Capsule can reduce NSS score and brain tissue injury after CIRI,and further activate autophagy by inhibiting the activation of PI3 K and up-regulating the expression of Beclin-1 protein,thus playing an antagonistic role against CIRI.
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