叶珩, 戚春建, 钱科卿. 抑瘤素M联合达卡巴嗪抑制黑色素瘤细胞B16的增殖[J]. 中国肿瘤临床, 2013, 40(24): 1540-1543. DOI: 10.3969/j.issn.1000-8179.20131151
引用本文: 叶珩, 戚春建, 钱科卿. 抑瘤素M联合达卡巴嗪抑制黑色素瘤细胞B16的增殖[J]. 中国肿瘤临床, 2013, 40(24): 1540-1543. DOI: 10.3969/j.issn.1000-8179.20131151
Heng YE, Chunjian QI, Keqing QIAN. Oncostatin M combined with dacarbazine inhibits proliferation of melanoma cell B16[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2013, 40(24): 1540-1543. DOI: 10.3969/j.issn.1000-8179.20131151
Citation: Heng YE, Chunjian QI, Keqing QIAN. Oncostatin M combined with dacarbazine inhibits proliferation of melanoma cell B16[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2013, 40(24): 1540-1543. DOI: 10.3969/j.issn.1000-8179.20131151

抑瘤素M联合达卡巴嗪抑制黑色素瘤细胞B16的增殖

Oncostatin M combined with dacarbazine inhibits proliferation of melanoma cell B16

  • 摘要:
      目的  通过体内外实验探讨抑瘤素M(OSM)联合达卡巴嗪(DTIC)对小鼠黑色素瘤细胞B16的抑制作用。
      方法  在体外分别采用MTT法和FCM法检测达卡巴嗪单药以及联合OSM对黑色素瘤B16细胞增殖和凋亡的影响;Hochest染色法检测达卡巴嗪单药以及联合OSM对黑色素瘤B16细胞的细胞核形态学变化,研究OSM联合DTIC对黑色素瘤B16细胞的抑制作用;体内实验将黑色素瘤细胞B16接种于小鼠,观察OSM、DTIC及DTIC联合OSM治疗对小鼠的成瘤性的影响。
      结果  体外实验中OSM、DTIC或DTIC联合OSM对黑色素瘤B16细胞的增殖抑制率分别为11.2±2.3%,25.3±4.6%和32.5±3.8%,差异具有统计学意义(P < 0.05),诱导黑色素瘤B16细胞的凋亡率分别为1.32±0.42%,10.64±2.13%和15.86±2.76%,差异具有统计学意义(P < 0.05)。在形态学上,DTIC联合OSM可明显引起细胞核破碎增加;在体内实验中,DTIC相对于对照组能明显抑制小鼠黑色素瘤的生长,DTIC联合OSM能增加DTIC的抑瘤作用。
      结论  OSM联合DTIC体外可以明显抑制黑色素瘤B16细胞增殖,诱导其凋亡,为黑色素瘤的治疗提供了一种新的可能性方案。

     

    Abstract:
      Objective  To observe and identify the inhibitory effect of oncostatin M (OSM) combined with dacarbazine (DTIC) on mouse melanoma cells B16 in vitro and in vivo.
      Methods  The inhibitory effect of OSM combined with DTIC on the proliferation and apoptosis of B16 melanoma cell line B16 were determined through MTT assay and flow cytometry, respectively. The change in nucleus morphology of B16 cells was observed under a fluorescence microscope by Hoechst staining method. The effects of single agents OSM and DTIC, as well as OSM–DTIC joint treatments, on tumor in mice in vivo were observed by inoculating B16 cells into C57 BL of six mice.
      Results  The OSM, DTIC, and combined OSM–DTIC treatments inhibited the proliferation of B16 cells by (11.2±2.3)%, (25.3±4.6)%, and (32.5±3.8)%, respectively (P < 0.05). Apoptosis of B16 occurred at (1.32±0.42)%, (10.64±2.13)%, and (15.86±2.76)%, respectively (P < 0.05). Cell morphology showed a significant increase in nuclear fragmentation, as proven by OSM-DTIC combined treatment. In the in vivo experiment, DTIC caused an apparent inhibition on the growth of mouse melanoma compared with the control group, and the joint treatment showed that the addition of OSM enhanced the tumor suppression effect of DTIC.
      Conclusion  OSM combined with DTIC has a synergistic effect that inhibits proliferation and apoptosis of B16 in vitro. This approach suggests a new potential treatment for melanoma.

     

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