细胞与分子免疫学杂志
細胞與分子免疫學雜誌
세포여분자면역학잡지
2009年
10期
929-931
,共3页
α干扰素%硫化砷%凋亡%端粒酶%K562细胞
α榦擾素%硫化砷%凋亡%耑粒酶%K562細胞
α간우소%류화신%조망%단립매%K562세포
IFN-α%arsenic sulfide%apoptosis%telomerase%K562 cells
目的:研究联合应用硫化砷和α干扰素是否可以增强对K562细胞的作用.方法:采用PCR-ELISA法测定端粒酶活性;流式细胞仪分析细胞凋亡.IFN-α和硫化砷的终浓度分别均为10 000 u/mL和0.6 mg/L.结果:单独应用IFN-α或硫化砷8 d,可以诱导37.8%和37%的K562细胞出现凋亡;同时应用IFN-α和硫化砷8 d或先单独应用IFN-α 3 d,再单独应用硫化砷5 d,K562细胞的凋亡率分别为59.9%和60.37%;端粒酶活性的抑制,单用硫化砷为71.3%,联合用药分别为81.2%和78.8%.结论:联合应用IFN-α和硫化砷较单独用药相比,可以显著提高K562细胞的凋亡,抑制细胞端粒酶活性.提示IFN-α司能促进硫化砷诱导K562细胞凋亡.
目的:研究聯閤應用硫化砷和α榦擾素是否可以增彊對K562細胞的作用.方法:採用PCR-ELISA法測定耑粒酶活性;流式細胞儀分析細胞凋亡.IFN-α和硫化砷的終濃度分彆均為10 000 u/mL和0.6 mg/L.結果:單獨應用IFN-α或硫化砷8 d,可以誘導37.8%和37%的K562細胞齣現凋亡;同時應用IFN-α和硫化砷8 d或先單獨應用IFN-α 3 d,再單獨應用硫化砷5 d,K562細胞的凋亡率分彆為59.9%和60.37%;耑粒酶活性的抑製,單用硫化砷為71.3%,聯閤用藥分彆為81.2%和78.8%.結論:聯閤應用IFN-α和硫化砷較單獨用藥相比,可以顯著提高K562細胞的凋亡,抑製細胞耑粒酶活性.提示IFN-α司能促進硫化砷誘導K562細胞凋亡.
목적:연구연합응용류화신화α간우소시부가이증강대K562세포적작용.방법:채용PCR-ELISA법측정단립매활성;류식세포의분석세포조망.IFN-α화류화신적종농도분별균위10 000 u/mL화0.6 mg/L.결과:단독응용IFN-α혹류화신8 d,가이유도37.8%화37%적K562세포출현조망;동시응용IFN-α화류화신8 d혹선단독응용IFN-α 3 d,재단독응용류화신5 d,K562세포적조망솔분별위59.9%화60.37%;단립매활성적억제,단용류화신위71.3%,연합용약분별위81.2%화78.8%.결론:연합응용IFN-α화류화신교단독용약상비,가이현저제고K562세포적조망,억제세포단립매활성.제시IFN-α사능촉진류화신유도K562세포조망.
AIM: To study if the effect of arsenic sulfide combined with IFN-α can be increased on K562 cells. METHODS: Telomerase activity was determined by PCRELISA. Flow cytometry was used to analyze the cell apoptosis. The final concentration of IFN-α and arsenic sulfide was 10 000 U/mL and 0.6 mg/L. RESULTS: The rates of apoptosis was 37.8% and 37% in K562 cells treated with IFN-α or arsenic sulfide alone for 8 days; The rates of apoptosis and inhibition of telomerase activity was 59.9% and 81.2% in K562 cells treated with IFN-α and arsenic sulfide simultaneously for 8 days, or 60.37% and 78.8% in K562 cells was treated with arsenic sulfide for 5 days after affected by IFN-α for 3 days. 71.3% telomerase activity was inhibited in K562 cells by arsenic sulfide alone for 8 days. CONCLUSION: Combination of arsenic sulfide and IFN-α can increase the apoptosis and inhibit the telomerase activity of K562 cells obviously comparing with the two drugs used alone. IFN-α maybe promote arsenic sulfide inducing apoptosis of K562 cells.