首都医科大学学报 ›› 2019, Vol. 40 ›› Issue (2): 186-190.doi: 10.3969/j.issn.1006-7795.2019.02.006

• 肿瘤的免疫治疗与代谢 • 上一篇    下一篇

β-羟丁酸对脑胶质瘤细胞增生糖酵解的影响

于春娜1, 江波2, 李文斌1, 陈峰1   

  1. 1. 首都医科大学附属北京天坛医院神经肿瘤综合治疗科, 北京 100050;
    2. 首都医科大学附属北京世纪坛医院胃肠外科/临床营养科, 北京 100038
  • 收稿日期:2019-01-17 出版日期:2019-03-21 发布日期:2019-04-15
  • 通讯作者: 李文斌 E-mail:liwenbin@ccmu.edu.cn
  • 基金资助:
    国家自然科学基金(81672888),北京双领学者西学中高级研修专项,北京高校高精尖学科建设项目(11920703),北京市科学技术委员会"首都临床特色应用研究"专项(Z181100001718127)。

Effects of β-hydroxybutyrate on the proliferation and glycolysis in glioma cells

Yu Chunna1, Jiang Bo2, Li Wenbin1, Chen Feng1   

  1. 1. Department of Neurooncology, Neurosurgery Center, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China;
    2. Department of Clinical Nutrition/Gastrointestinal Surgery, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China
  • Received:2019-01-17 Online:2019-03-21 Published:2019-04-15
  • Supported by:
    This study was supported by National Natural Science Foundation of China (81672888),National Natural Science Foundation of China,Senior research project of Beijing double leading scholars in Western medicine studies,Construction Project of Top Disciplines in Beijing Universities(11920703),Beijing Municipal Science & Technology Commission(Z181100001718127).

摘要: 目的 本研究探讨生酮饮食(ketogenic diet,KD)代谢产物之一的β-羟丁酸(β-hydroxybutyrate,β-HB)对脑胶质瘤细胞增生及糖酵解水平的影响,研究KD治疗脑胶质瘤的机制。方法 用不同浓度的β-HB处理脑胶质瘤细胞系U87及LN229后,通过CCK8实验检测细胞增生,糖酵解压力测试检测细胞糖酵解能力,实时定量聚合酶链式反应(real-time quantitative polymerase chain reaction,RT-qPCR)法检测c-myc基因表达,Western blotting法检测c-myc蛋白表达。结果 β-HB对LN229及U87细胞的生长抑制随着药物浓度增加而升高,呈现出剂量依赖性;与未处理组相比,实验组细胞糖酵解水平及最大糖酵解能力明显降低;经过β-HB处理后细胞c-myc表达降低。结论 β-HB可能通过c-myc抑制脑胶质瘤细胞U87及LN229的糖酵解能力,从而影响细胞增生。提示KD可以作为治疗脑胶质瘤的方法之一。

关键词: 脑胶质瘤, β-羟丁酸, 生酮饮食, 糖酵解

Abstract: Objective To investigate the effects of β-hydroxybutyrate (β-HB), one of the ketogenic diet (KD) metabolites, on the proliferation and glycolysis of glioma cell lines to reveal the mechanisms of KD in the treatment of glioma. Methods After treated with different concentrations of β-HB, the proliferation of glioma cell lines U87 and LN229 was detected with CCK8 assay and glycolysis ability of cells was measured with glycolysis stress test. Further, the transcription factor c-myc expression was detected with Western blotting and real-time quantitative polymerase chain reaction (RT-qPCR). Results β-HB can inhibit the proliferation of glioma cells in a dose-dependent manner. Compared with the untreated group, the glycolysis level and maximum glycolytic capacity was decreased and the expression of c-myc was down-regulated in the experimental groups. Conclusion β-HB can affect the glycolytic capacity of glioma cell lines U87 and LN229 through c-myc, and thus inhibit cell growth. It is suggested that KD can be used as an efficacious therapy agent for glioma.

Key words: glioma, β-hydroxybutyrate, ketogenic diet, glycolysis

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