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作 者:杨希营 王古岩[1,2] 张丛雅 陈一萌 杜英杰 YANG Xi-ying;WANG Gu-yan;ZHANG Cong-ya;CHEN Yi-meng;DU Ying-jie(Department of Anesthesiology,Fuwai Hospital,State Key Laboratory of Cardiovascular Disease,National Center for Cardiovascular Disease,Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing 100037,China;Department of Anesthesiology,Beijing Tongren Hospital,Capital Medical University,Beijing 100730,China)
机构地区:[1]国家心血管病中心中国医学科学院北京协和医学院阜外医院麻醉科,北京市100037 [2]首都医科大学附属北京同仁医院麻醉科,北京市100730
出 处:《中国分子心脏病学杂志》2020年第6期3644-3646,共3页Molecular Cardiology of China
基 金:国家自然科学基金(81770414,81970344)。
摘 要:目的研究人肾小管上皮细胞深低温暴露诱导的自噬对凋亡的作用。方法建立HK2细胞和HK2-GFP-LC3稳定细胞系体外深低温暴露模型,分别用荧光显微镜检测自噬和凋亡。结果深低温暴露诱导了HK2-GFP-LC3细胞持续性自噬,抑制细胞自噬增加了低温暴露后48 h的细胞凋亡。结论自噬在深低温暴露诱导的人肾小管上皮细胞凋亡中发挥保护作用。Objective To study the effect of autophagy on apoptosis in HK2 cells induced by deep hypothermic exposure.Methods A Hk2-GFP-LC3 cell deep hypothermic exposure model was established in vitro.Fluorescence microscopy was used to detect autophagy and apoptosis respectively.Results Autophagy was induced and persisted for hours by deep hypothermic exposure in HK2-GFP-LC3 cells.Inhibition of autophagy enhanced caspase 3 associated apoptosis.Conclusion Autophagy plays a protective role in the process of apoptosis induced by deep hypothermic exposure.
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