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γ-干扰素与维拉帕米联合逆转人肺癌细胞系的多药耐药 被引量:3

Combined Use of VPL、INF-γand DDP to Revert the Multidrug Resistance of Lung Cancer Cell Line
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摘要 目的 探讨逆转人肺癌耐药系HTB - 5 6R耐药性的可行性。方法 采用MTT比色法研究钙通道阻滞剂维拉帕米和人类重组γ -干扰素对DDP细胞毒性在人类肺癌细胞系HTB - 5 6R上的的影响。结果 γ -干扰素与维拉帕米能部分恢复HTB - 5 6R对顺铂 (DDP)的敏感性。当维拉帕米浓度 >4mg/L时 ,能明显增加DDP的细胞毒性 ,耐药株的抑制率 >19.0 % (P <0 .0 5 )。γ -干扰素浓度 >4.0× 10 6 U/L时 ,也能达到此效果 ,细胞抑制率 >3 6.9% (P <0 .0 5 )。联合两药比单独使用有更好的效果 ,维拉帕米为 2mg/L、γ -干扰素为 2 .0× 10 6 U/L时 ,细胞抑制率就达 3 6.9% (P <0 .0 1)。不论单独使用还是联合使用逆转效果均呈剂量效应。结论 γ -干扰素与维拉帕米能逆转HTB - 5 6R的耐药性 ,而且联合使用有更好的效果。 Objective To probe into the possibility of reversion of the drug resistance in HTB-56R. Methods The effect of VPL, an antagonists to calcium channel and INF-γ(recombinant human γ-interferon) on the cytotoxicity of DDP in human lung cancer cell line HTB-56R were studied in vitro by MTT colorimetric assay. Results The results showed that drug sensitivty to DDP was partly reestablished by VPL or INF-γ. VPL at concertration above 4mg/L could significantly enhance the cytotoxicity of DDP, the lung cancer cell line inhibition rate >19.0% ( P <0.05).INF-γ at concertration above 4.0×10 6U/L could also significantly enhance the cytotoxicity of DDP, the inhibition rate >36.9% ( P <0.05). Combinatin of VPL and INF-γ had better result than either of the two alone, the dose of VPL at 2mg/L 、INF-γ at 2.0×10 6U/L, the inhibition rate being 36.9% ( P <0.01). The extent of enhancement is correspondingly increased as the dose is increased. Conclusion VPL and INF-γ can revert the multidrug resistance of HTB-56R. Combination of VPL and INF-γ have better result than either of the two alone.
出处 《苏州大学学报(医学版)》 CAS 2003年第1期16-18,21,共4页 Suzhou University Journal of Medical Science
关键词 肺癌细胞株 逆转多药耐药 DDP VPL INF-Γ lung cancer cell line revert the multidrug resistance DDP VPL INF-γ
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  • 1刘沪丽 杜平.人γ干扰素与人α干扰素的抗肿瘤细胞增殖作用的比较[J].中国免疫学杂志,1989,5:6-6.

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  • 1李建人,赵彼得,罗沈如,马爱敏.高热合并化疗放疗对人结肠癌细胞的作用[J].中华理疗杂志,1995,18(3):131-133. 被引量:8
  • 2宋鹏,段蕴铀,杨建军,黄友章,雷军慧.维拉帕米对外照射导致的小细胞肺癌细胞系耐药性的逆转作用[J].解放军医学杂志,2007,32(4):365-367. 被引量:2
  • 3Pere z-Tomas R. Muhidrug resistance: retrospect and prospects in anti-cancer drug treatment[J]. Curr Med Chem, 2006, 13(16):1859-1876.
  • 4Chudziuski W, Niderla J, Lasiecka Z, et al. P-glycoprotein expression influences the result of ^99mTc-MIBI scintigraphy in tertiary hyperparathyroidism [J]. Int J Mol Med, 2005, 16(2):215-219.
  • 5Dyszlewski M, Blake HM, Dahlheimer JL, et al. Characterization of a novel ^99Tc^m-carbonyl complex as a functional probe of MDR1 P-glycoprotein transport activity[J]. Mol Imaging, 2002, 1(1): 24-35.
  • 6Marian T, Balkay L, Szabo G, et al. Biphasic accumulation kinetics of [^99mTc]-hexakis-2-methoxyisobutyl isonitrile in tumour cells and its modulation by lipophilic P-glycoprotein ligands[J]. Eur J Pharm Sci, 2005, 25(2/3):201-209.
  • 7Kinuya S, Bai J, Shiba K, et al. ^99mTc-sestamibi to monitor treatment with antisense oligodeoxynucleotide complementary to MRP mRNA in human breast cancer cells [J]. Ann Nucl Med, 2006,20(1):29-34.
  • 8Van de Wiele C, Signore A, Dierckx RA. Peptide receptor imaging: advances in the diagnosis of pulmonary diseases [J]. Am J Respir Med, 2002,1(3): 177-183.
  • 9Fonti R, Del Vecchio S, Zannetti A, et al. Functional imaging of multidrug resistant phenotype by ^99mFc-MIBI scan in patients with multiple myeloma [J]. Cancer Biother Radiopharm, 2004,19(2):165-170.
  • 10Thorgeirsson SS, Huber BE, Sorrell S, et al. Expression of the multidrug- resistant gene in hepatocarcinogenesie and regenerating rat liver [J]. Science, 1987,236(4805): 1120-1122.

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