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作 者:刘艳丽 梁小裕 周妍妍[3] LIU Yanli;LIANG Xiaoyu;ZHOU Yanyan(Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University,Taizhou 317000,Zhejiang,China;Luqiao Hospital,Taizhou Enze Medical Center(Group),Taizhou 318050,Zhejiang,China;Heilongjiang University of Chinese Medicine,Harbin 150040,Heilongjiang,China)
机构地区:[1]台州医院,浙江台州317000 [2]台州恩泽医疗中心(集团)路桥医院,浙江台州318050 [3]黑龙江中医药大学,黑龙江哈尔滨150040
出 处:《辽宁中医杂志》2023年第2期149-152,I0004,I0005,共6页Liaoning Journal of Traditional Chinese Medicine
基 金:国家自然科学基金面上项目(81774197);台州市科技计划项目(20ywb78)。
摘 要:目的 探讨细叶远志皂苷(tenuifolin, TEN)对Aβ_(25-35)(淀粉样蛋白片段)诱导PC12细胞损伤对线粒体自噬的影响。方法 设立不同浓度TEN组,干预Aβ_(25-35)诱导PC12细胞损伤模型,MTT及流式细胞术检测确立细胞保护浓度。实验分为空白组、模型组、TEN组。JC-1测线粒体膜电位,Western Blot检测PINK1、Parkin、LC3II/I、p62蛋白的表达。结果 与空白组比较,模型组线粒体膜电位下降,PINK1、Parkin、 LC3II/I和蛋白表达升高,P62蛋白表达下降;与模型组比较,TEN组细胞线粒体膜电位上调,PINK1、Parkin和LC3II/I蛋白表达降低,P62蛋白表达升高。结论 细叶远志皂苷能减轻Aβ_(25-35)诱导的PC12细胞损伤,其机制可能与调控PINK1-Parkin介导的粒体自噬途径相关。Objective To investigate the effect of tenuifolin on PINK1/Parkin mediated mitochondrial autophagy in PC12 cells induced by Aβ_(25-35).Methods Different concentrations of tenuifolin groups were set up to intervene Aβ_(25-35)-induced PC12 cell injury model, and the cell protection concentration was determined by MTT and flow cytometry.The experiment was divided into blank group, model group and polygala saponin group.Mitochondrial membrane potential was measured by JC-1.The expressions of PINK1,Parkin, LC3II/I and P62 protein were detected by Western Blot.Results Compared with those of the blank group, the mitochondrial membrane potential decreased, the expressions of PINK1,Parkin, LC3II/I and protein increased, and P62 protein expression decreased in the model group.Compared with those of the model group, the mitochondrial membrane potential was up-regulated, the expressions of PINK1,Parkin and LC3II/I protein were decreased, and P62 protein expression was increased in the tenuifolin group.ConclusionTenuifolin can reduce Aβ_(25-35)-induced PC12 cell damage, and the mechanism may be related to the regulation of PINK1-Parkin mediated granular autophagy pathway.
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