CAJ | 학술논문

目的：研究大黄素乙酰化物作用鼻咽癌CNE-1细胞后，其线粒体损伤及其与线粒体自噬的关系。方法以5 mg·L-1及10 mg·L-1大黄素乙酰化物作用鼻咽癌CNE-1细胞，通过透射电镜观察大黄素乙酰化物导致鼻咽癌CNE-1细胞自噬体形成的超微结构；激光共聚焦显微镜测定线粒体膜电位、细胞内钙离子、细胞内活性氧的浓度变化及线粒体自噬的活性。结果与空白对照组比较，两个实验组细胞都出现线粒体损伤以及线粒体自噬体。大黄素乙酰化物作用后的细胞线粒体膜电位降低（P<0.05）；细胞内游离的钙离子浓度升高（P<0.05）；细胞内活性氧增加（P<0.05），且呈剂量依赖性。经线粒体与溶酶体示踪分析，可见大黄素乙酰化物作用的实验组均出现酸性溶酶体增殖，其中包含线粒体探针标记的线粒体碎片等典型的自噬特征，且增加的趋势呈剂量效应关系。结论大黄素乙酰化物可致鼻咽癌CNE-1细胞线粒体损伤，并与线粒体自噬密切相关。
목적：연구대황소을선화물작용비인암CNE-1세포후，기선립체손상급기여선립체자서적관계。방법이5 mg·L-1급10 mg·L-1대황소을선화물작용비인암CNE-1세포，통과투사전경관찰대황소을선화물도치비인암CNE-1세포자서체형성적초미결구；격광공취초현미경측정선립체막전위、세포내개리자、세포내활성양적농도변화급선립체자서적활성。결과여공백대조조비교，량개실험조세포도출현선립체손상이급선립체자서체。대황소을선화물작용후적세포선립체막전위강저（P<0.05）；세포내유리적개리자농도승고（P<0.05）；세포내활성양증가（P<0.05），차정제량의뢰성。경선립체여용매체시종분석，가견대황소을선화물작용적실험조균출현산성용매체증식，기중포함선립체탐침표기적선립체쇄편등전형적자서특정，차증가적추세정제량효응관계。결론대황소을선화물가치비인암CNE-1세포선립체손상，병여선립체자서밀절상관。
Objective To explore the relationship between mitochondrial damage and mitophagy in nasopharyngeal carcinoma CNE-1 cells treated with acetylated emodin derivative. Methods CNE-1 cells were divided into a control group and groups treated with 5 or 10 mg·L-1 of acetylated emodin derivative.After treatment,autophagosome ultrastructure was analyzed by transmission electron microscopy,while mitochondrial membrane potential and levels of intracellular free calcium ion and reactive oxygen species were measured by confocal microscopy. Results Cells treated with acetylated emodin derivative showed mitochondrial damage and the presence of mitophagosomes,which were not observed in control cells.The emodin derivative also led to a significant decrease in mitochondrial membrane potential and increases in levels of intracellular free calcium ion and reactive oxygen species (P<0.05);these effects were dose-dependent. Analyzing mitochondrial and lysosome markers of treated cells revealed typical mitophagic features, including acidic lysosomal proliferation and lysosomes containing mitochondrial remnants labeled with Mito Tracker Green. The abundance of these features was also dose-dependent. Conclusion The acetylated emodin derivative can cause mitochondrial damage in nasopharyngeal carcinoma CNE-1 cells,perhaps through a mechanism closely related to mitophagy.