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金雀异黄素诱导K562和K562/ADM细胞的凋亡作用 被引量:1

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摘要 目的探讨金雀异黄素(GS)对人红白血病细胞系K562与其多药耐药细胞系K562/ADM的生长抑制、诱导凋亡作用及其可能的作用机制。方法不同浓度的GS处理K562与K562/ADM细胞后,用MTT比色法检测生长增殖作用,流式细胞术检测凋亡,免疫细胞化学ABC法分析Bcl-2和Bax蛋白的表达。结果 GS对K562及K562/ADM细胞均有很强的生长抑制作用。同一浓度下GS诱导K562/ADM细胞凋亡率明显低于K562细胞。不同浓度GS对K562细胞的Bax蛋白呈强阳性表达,Bcl-2蛋白实验组同对照组比较颜色无明显变化;而在K562/ADM细胞中,Bcl-2在实验组和对照组中均强表达,但Bax的表达均无明显变化。结论 K562细胞对GS的反应比K562/ADM细胞敏感;GS诱导K562细胞Bax蛋白高表达可能是GS诱导K562细胞凋亡的机制之一,而K562/ADM细胞的耐药性和凋亡抑制可能与Bcl-2蛋白高表达有关。
出处 《中国老年学杂志》 CAS CSCD 北大核心 2014年第9期2516-2518,共3页 Chinese Journal of Gerontology
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