人参皂甙Rh2对人胶质瘤细胞内钙离子浓度的影响
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  • 英文篇名:Research on the effect of ginsenoside Rh2 on intracellular calcium concentration of human brain glioma cells
  • 作者:吴章泽 ; 王一芳 ; 王正伟 ; 陈昌
  • 英文作者:WU Zhang-ze;WANG Yi-fang;WANG Zheng-wei;CHEN Chang;Department of Neurology,Air Force Hospital of Eastern Theater Command;
  • 关键词:人参皂甙Rh2 ; 人胶质瘤细胞 ; 细胞内钙离子浓度 ; L型电压依赖性钙离子通道 ; Cav1.2
  • 英文关键词:ginsenoside Rh2;;human brain glioma cells;;intracellular calcium concentration;;L-type calcium channel;;Cav1.2
  • 中文刊名:DNGY
  • 英文刊名:Military Medical Journal of Southeast China
  • 机构:东部战区空军医院神经科;
  • 出版日期:2019-01-20
  • 出版单位:东南国防医药
  • 年:2019
  • 期:v.21;No.236
  • 语种:中文;
  • 页:DNGY201901003
  • 页数:5
  • CN:01
  • ISSN:32-1713/R
  • 分类号:18-22
摘要
目的观察人参皂甙Rh2对人胶质瘤细胞内钙离子浓度的影响。方法实验分为对照组和人参皂甙Rh2组,对照组应用常规培养基培养人胶质瘤细胞株U87MG,人参皂甙Rh2组在常规培养基中人参皂甙Rh2的浓度为20μg/m L,利用激光共聚焦显微镜和流式细胞仪检测各组培养的人胶质瘤细胞内钙离子浓度,再利用Western blot技术检测人胶质瘤细胞Cav1.2蛋白的表达,最后利用膜片钳技术检测人胶质瘤细胞L型电压依赖型钙离子通道的功能。结果人参皂甙Rh2处理U87MG细胞后,细胞内钙离子浓度是对照组的2.5倍(P<0. 05);人参皂甙Rh2培养后胶质瘤细胞Cav1.2蛋白表达量是对照组的1.5倍(P<0. 05),且L型电压依赖性钙离子通道功能增强。结论人参皂甙Rh2可通过增加胶质瘤细胞Cav1.2表达和L型电压依赖性钙离子通道的功能促进细胞内游离钙离子浓度的增加,从而诱导人胶质瘤细胞的凋亡。
        Objective To investigate the effect of ginsenoside Rh2 on intracellular calcium concentration of human brain glioma cells and its mechanism. Methods Human U87 MG brain glioma cells were cultured in conventional medium( control group)and in conventional medium with 20 μg/m L ginsenoside Rh2( experimental group). We tested the intracellular calcium concentration of human brain glioma cells by laser scanning confocal microscope and flow cytometry. The expression of Cav1.2 was measured by the Western blotting. And the function of L-type calcium channel was measured by patch clamp. Results The treatment of ginsenoside Rh2 increased the intracellular calcium concentration of human brain glioma cells,promoted the expression of Cav1.2 and facilitated the function of L-type calcium channel. Conclusion Ginsenoside Rh2 increases the intracellular calcium concentration of human brain glioma cells by promoting the expression of Cav1.2 and facilitating the function of L-type calcium channel.
引文
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