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目的观察雷公藤内酯醇在体外抑制人黑素瘤细胞A375增殖和迁移的能力及对细胞表面趋化因子受体CCR7表达的影响情况,初步分析其作用机制。方法用CCK-8比色试剂盒检测雷公藤内酯醇对A375细胞增殖的作用,Transwell微孔隔离小室迁移实验检测雷公藤内酯醇对A375细胞体外迁移能力的影响,Western blot法检测雷公藤内酯醇对A375细胞CCR7蛋白表达的影响。结果雷公藤内酯醇以剂量依赖方式抑制A375细胞的增殖,24h的IC50值为0.20μg/mL;雷公藤内酯醇能显著地抑制A375细胞的体外迁移能力(P<0.01),侵袭抑制率约为82.84%;经不同浓度雷公藤内酯醇(0μg/mL,0.2μg/mL和0.4μg/mL)处理后,A375细胞中CCR7蛋白表达呈明显下降趋势(P<0.05)。结论雷公藤内酯醇具有抗A375细胞增殖和体外迁移能力的作用,其机制可能与下调其表面趋化因子受体CCR7的表达相关,并且该作用呈一定的浓度依赖性。
Objective To observe the effects of triptolide on the proliferation and migration of human melanoma cell line A375 and its effect on the expression of chemokine receptor CCR7 on cell surface in vitro and its mechanism of action. Methods The effect of triptolide on the proliferation of A375 cells was detected by CCK-8 colorimetric kit. The migration of A375 cells was detected by Transwell micropore migration assay. The effects of triptolide On A375 cell CCR7 protein expression. Results Triptolide inhibited the proliferation of A375 cells in a dose-dependent manner with an IC50 value of 0.20 μg / mL for 24 h. Triptolide significantly inhibited the in vitro migration of A375 cells (P <0.01), and the invasion inhibition rate was about 82.84%. After treatment with different concentrations of triptolide (0μg / mL, 0.2μg / mL and 0.4μg / mL), the expression of CCR7 in A375 cells decreased significantly (P <0.05). Conclusion Triptolide can inhibit the proliferation and migration of A375 cells in vitro. The mechanism may be related to the down-regulation of the expression of CCR7, a chemokine receptor, in a concentration-dependent manner.