赖氨匹林对黑色素瘤B16细胞的增殖抑制作用

Inhibitory Effect of Aspisol on Proliferation of Melanoma B16 Cells

[目的]探讨非甾体抗炎药赖氨匹林(Aspisol)对小鼠黑色素瘤细胞株B16的增殖抑制作用及其可能的机制。[方法]应用MTT比色法分析细胞生长抑制作用,流式细胞技术测定凋亡率,应用Western blot分别检测COX-2蛋白和凋亡相关蛋白Bcl-2、Bax的表达。[结果]2～8mmol/L赖氨匹林可抑制B16细胞的生长,且其作用具有剂量和时间依赖性(P<0.01)。赖氨匹林(2、4、8mmol/L)作用24h后诱导B16细胞的凋亡率分别为5.05%±1.23%、9.25%±1.46%、14.80%±1.98%,并呈浓度依赖性;与对照组(0.18%±0.13%)比较差异有显著性(P<0.01)。赖氨匹林抑制B16细胞COX-2蛋白的表达(P<0.05);赖氨匹林可促进Bax蛋白表达(P<0.05),但抑制Bcl-2的表达(P<0.05)。[结论]赖氨匹林通过影响COX-2蛋白的表达,调节凋亡相关蛋白表达,抑制B16细胞增殖。

[Purpose] To explore the inhibitory effect and mechanism of Aspisol, a kind of non-steroidal anti-inflammatory drugs （NSAIDs） on the proliferation of melanoma B16 ceils. [Methods] The inhibitive effects of Aspisol on B16 cells were observed with the MTT assay. The cell apoptosis was detected by flow cytometry. The COX-2, Bax and Bel-2 protein expressions were detected by Western blot method. [Results] Aspisol of 2-8mmol/L could inhibit the growth of B16 cells in a time-and dose-dependent manner （P〈0.01）. The apoptotic rate of B16 cells exposured to different concentrations of Aspisol （2,4,8mmool/L） for 24h was 5.05%±1.23%, 9.25%±1.46%, 14.80%±1.98%, respectively, in a dose-dependent manner and there was significantly difference compared to control group （0.18%＋0.13%） （P〈0.01）. The expression of COX-2 and Bcl-2 protein in B16 cells was down-regulated（P〈0.05） and Bax expression up-regulated by Aspisol（P〈0.05）. [Conclusion] Aspisol can effect the expression of COX-2 protein and induce the expression of apoptosis related proteins to inhibit the proliferation of B16 cells.