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应用膜片钳技术探讨阿霉素对骨肉瘤(OS-732)及其耐药细胞(R-OS-732)钙离子通道的影响 被引量：3

Study on the Effect of ADM on Ca2 + Channel of OS - 732 and R - OS - 732 Cells with Patch Clamp Technique
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摘要 目的：应用全细胞膜片钳技术测定ＯＳ－７３２及Ｒ－ＯＳ—７３２两种细胞的反应钙离子通道的钙离子电流，同时测定阿霉素单独及与异博定共同作用对两种细胞钙离子电流的影响。结果；ＯＳ－７３２细胞的峰值电流为（－０．２３０６±０．０１）ｎＡ（ｎ＝１０），Ｒ－ＯＳ－７３２为（－０．３０１４９±０．０４）ｎＡ（ｎ＝１０），二者相比差异显著（Ｐ＜０．０５）。阿霉素单独作用，随阿霉素浓度的增大（１～１００μｇ／ｍｌ），ＯＳ－７３２细胞峰值电流由（－０．２０６６９±０．０９）ｎＡ降到（－０．１０７０３±０．０６）ｎＡ，降低幅度为４５．１７％。Ｒ－ＯＳ－７３２细胞的峰值电流由（－０．２８４３５± ０．０４）ｎＡ降至（－０．２３８７３±０．０３）ｎＡ，降低幅度为７９．１８％。异搏定单独作用，当异搏定浓度为ｌμｇ／ｍｌ时，ＯＳ－７３２细胞的峰值电流降低幅度为５７．４％；Ｒ－ＯＳ－７３２细胞的降低幅度为５０．８１％。当阿霉素浓度为１０μｇ／ｍｌ，加入浓度为１μｇ／ｍｌ的异博定时。对于ＯＳ－７３２细胞降低幅度为７３．４４％，而Ｒ－ＯＳ－７３２细胞则为９１．３２％。 Objective: To study the effect of ADM on Ca2 + channel of OS - 732 cells and R - OS - 732 cells. Methods: The original current of both OS - 732 cells and R - OS - 732 cells had been recorded by using the patch clamp technique, the peak current was obtained through the current voltage relationship curve. Results: The peak current of OS - 732 cells and R - OS - 732 cells were (-0.23696±0.01) nA (n =10)and (- 0.30149 ±0.04)nA(n = 10)respectively. The difference between them was significant (P <0.05). The peak current of both two kinds of cells decreased with the increasing of the concentration of ADM, for OS-732 cells, it decreased from( -0.20669 ± 0.09)nA to( -0.10703 ± 0.06)nA, while for R - OS-732 cells it decreased from( - 0.28435 ± 0.04)nA to ( - 0.23837 ± 0.03)nA. The Verapamil can decrease the peak current of both kinds of cells, for OS - 732 cells it decreased 57 .4%, while for R - OS - 732 cells it decreased 50.81%. The ADM together with Verapamil can decrease the peak current of OS - 732 cells and R - OS - 732 cells respectively. For OS - 732 cells it decreased 73. 44%, while for R - OS - 732 cells decreased 91 .32%. Conclusion: Both ADM and Verapamil can inhibit the Ca2 + channel of OS - 732 cells and B - OS - 732 cells. For R - OS - 732 cells it behaved more obvious. The inhibition of ADM together with Verapamil to the Ca2 + channel of OS - 732 cells and R -OS - 732 cells was higher than that of ADM or Verapamil alone, but the effect was not a simple addition of effects of ADM and Verapamil.
作者 谷贵山 徐莘香
机构地区 白求恩医科大学第一临床学院骨科
出处 《生物医学工程与临床》 CAS 2000年第2期77-81,共5页 Biomedical Engineering and Clinical Medicine
基金 吉林省科委资助项目
关键词 阿霉素 钙离子通道 耐药细胞 异搏定 骨肉瘤 异博定 抑制作用 全细胞膜片钳技术 反应 同时测定 Osteosarcoma Electrophysiology Multidrug resistance Patch clamp technique
分类号 R738.1 [医药卫生—肿瘤]
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同被引文献40

  • 1黄昌州,张宗明,裘法祖.缺血再灌注损伤对大鼠肝细胞钙池操纵的钙通道电流的影响及药物拮抗[J].世界华人消化杂志,2005,13(6):739-742. 被引量：8
  • 2李福春,谷贵山,孙大辉,车明学,张德宝,杨震.瞬时性受体电位通道香草酸受体5、6与骨代谢的关系[J].中国组织工程研究与临床康复,2007,11(19):3837-3841. 被引量：1
  • 3Rychkov G, Brereton HM, Harland ML, et al. Plasma membrane Ca^2+ release-activated Ca^2+ channel with a high selectivity for Ca^2+ identified by patch-clamp recording in rat liver cells. Hepatology, 2001, 33:938-947.
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  • 5Bootman MD, Collins TJ, Mackenzie L, et al. 2-aminoethoxydiphenyl borate (2-APB) is a reliable blocker of store-operated calcium entry but an inconsistent inhibitor of ins ( 1,4,5) P3-induce Ca^2+ release. FASEB J, 2002, 16:1145-1150.
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  • 7Gregory RB, Rychkov G, Barritt GJ. Evidence that 2-Aminoethoxydiphenyl Borate is a novel inhibitor of store-operated Ca^2+ channels in liver cells, and act through a mechanism which does not involve inositol trisphosphate receptors. Biochem J, 2001, 354 : 285 -290.
  • 8Gregory R.B, Barritt GJ. Evidence that Ca^2+ release-activated Ca^2+ channel in rat hepatocytes are required for the maintenance of hormoneinduce Ca^2+ oscillation. Biochem J, 2003, 370:695-702.
  • 9Clair C, Tran D, Boucherie S, et al. Hormone receptor gradients supporting directional Ca^2+ signals: direct evidence in rat hepatocytes. J Hepatol, 2003, 39 : 489-495.
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生物医学工程与临床
2000年 第2期

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