硫化砷诱导K562细胞凋亡中Bcl┐2和Bax的表达 _医学论文.docVIP

硫化砷诱导K562细胞凋亡中Bcl┐2和Bax的表达 _医学论文 硫化砷诱导K562细胞凋亡中Bcl┐2和Bax的表达 _医学论文 【关键词】 白血病 关键词: Bcl-2砷化物凋亡雄黄白血病，髓样，慢性 摘 要:目的 研究Bcl-2和Bax在硫化砷诱导的K562细胞凋亡中的表达，探讨其在硫化砷诱导的细胞凋亡中的作用. 方法 K562细胞经一定剂量硫化砷作用特定时间后，MTT法检测细胞生长、增殖状态，光镜及透射电镜下观察细胞形态及凋亡情况，S-P免疫组化染色检测Bcl-2、Bax的表达并进行图像分析. 结果 硫化砷对K562细胞生长增殖有时间剂量依赖性抑制作用175～1400μg#12539L-1 硫化砷作用18～144h后，K562细胞出现凋亡细胞的形态学改变免疫组化染色表明K562细胞低表达Bcl-2蛋白（A值为0.152±0.023，阴性对照A值0.108±0.012），硫化砷处理后对其表达无明显影响（A值为0.138±0.028，Pgt0.05）.硫化砷作用后，Bax蛋白的表达量A值由0.240±0.013增加到0.316±0.021（0.01）. 结论 硫化砷可抑制K562细胞的生长和增殖并诱导其发生凋亡，其机制可能与Bax蛋白上调有关. 　　Keywords:proto-oncogene proteins c-Bcl-2arsenicalsapoptosisrealgarleukemia，myeloid，chronic 　　Abstract:AIM To study the expression and the effects of Bcl-2and Bax protein in apoptosis of K562cell induced by ar-senic sulfide.METHODS After being incubated in culture medium containing variable levels of arsenic sulfide，cell growth and proliferation of K562cell was analyzed with MTT assayapoptosis was detected with cell morphology by light and transmission electron microscopy.The expression　of Bcl-2and Bax protein was determined with S-P immuno-histochemical stainning and imaging analysis.RESULTS After the treatment，cell growth and proliferation of K562cell was inhibited in a dose-and time-dependent manner.Morphologically，after treatment with175to1400μg#12539L-1 of arsenic sulfide for18to144h，K562cells presented some features of apoptosis.The baseline Bcl-2expression of K562cell was very low（A:0.152±0.023）while the absorbance（optical density）value（A）of negative control was0.108±0.012.No significant difference was found after the treat-ment（A:0.138±0.028）（Pgt0.05），but the expression of Bax protein in K562cells co-cultured with arsenic sulfide（A:0.316±0.021）was increased，compared with the untreated（A:0.240±0.013）（0.01）.CONCLUSION Arsenic sulfide could inhibit growth and proliferation of K562cell and induce its apoptosis.These effects may be correlated with the up-regulation of Bax protein. 　　0 引言 　　雄黄在我国传统医学中有悠久的历史，主要成分为硫化砷（As4 S4 和