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目的研究硫化砷对骨肉瘤细胞生长和凋亡的影响,并探讨其可能的机制。方法应用噻唑蓝(MTT)比色法检测细胞生长抑制率、倒置显微镜观察细胞形态、AnnexinⅤ法检测细胞凋亡、逆转录聚合酶链反应(RTPCR)法检测bcl2及bax基因的表达,观察硫化砷对骨肉瘤细胞株MG63诱导凋亡的作用。结果硫化砷可明显抑制MG63细胞的增殖,1.0mg/L浓度的硫化砷作用24h后,MG63细胞的抑制率可达26.43%。倒置显微镜观察被硫化砷抑制的MG63细胞呈典型的凋亡改变,流式细胞仪检测凋亡率与硫化砷处理时间、处理浓度呈正相关。在硫化砷的作用下,MG63细胞的bcl2表达下调,而bax表达无明显改变。结论硫化砷可有效地诱导骨肉瘤细胞凋亡,bcl2表达下调是诱导细胞凋亡的重要机制。
Objective To study the effect of arsenic sulfide on the growth and apoptosis of osteosarcoma cells and to explore its possible mechanism. Methods Cell growth inhibition rate was measured by MTT colorimetric assay, cell morphology was observed by inverted microscope, apoptosis was detected by AnnexinⅤ method, and bcl2 and bax gene expression was detected by reverse transcriptase polymerase chain reaction (RTPCR) On osteosarcoma cell line MG63 induced apoptosis. The results of arsenic sulfide can inhibit the proliferation of MG63 cells significantly. After treated with 1.0mg / L arsenic sulfide for 24h, the inhibition rate of MG63 cells reached 26.43%. Inverted microscope was used to observe the typical apoptosis of MG63 cells inhibited by arsenic sulfide. The apoptotic rate of flow cytometry was positively correlated with the time and concentration of arsenic sulfide treatment. Under the action of arsenic sulfide, the expression of bcl2 in MG63 cells was down-regulated, while the expression of bax did not change significantly. Conclusion Arsenic sulfide can effectively induce apoptosis of osteosarcoma cells. The down-regulation of bcl-2 expression is an important mechanism of apoptosis induction.