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丁酸钠和氯高铁血红素诱导K562细胞分化的信号转导机制

Signal transduction mechanisms of differentiation induced by sodium butyrate and Hemin in K562 cells
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摘要 目的 探讨丁酸钠和氯高铁血红素 (hemin ,Hm)诱导K5 6 2细胞向红系分化的信号转导机制。方法 采用台盼蓝拒染法观察丁酸钠和Hemin对K5 6 2细胞生长曲线的影响 ;流式细胞仪进行细胞周期分析 ;联苯胺染色检测药物诱导K5 6 2细胞向红系分化作用。结果 丁酸钠和Hemin呈时间和剂量依赖方式诱导K5 6 2细胞向红系分化 ;ERK抑制剂PD980 5 9增加丁酸钠、降低Hemin诱导的联苯胺阳性率JNK抑制剂SP6 0 0 12 5未影响丁酸钠却降低Hemin的诱导分化作用。结论 在K5 6 2细胞向红系分化过程中 ,ERK正性调节Hemin、负性调节丁酸钠的诱导分化作用 ; Aim To explore the signal transduction mechanisms of erythroid differentiation induced by sodium butyrate and Hemin in K562 cells. Methods The percentage of viable cells was determined by trypan blue exclusion. Ce ll cycle distribution was studied after DNA staining by propidium iodide. Erythr oid differentiation was tested by benzidine-staining.Results Sodium butyrate and Hemin induced erythroid differentiation in a dose and t ime- dependent fashion in K562 cells. ERK inhibitor PD98059 enhanced sodium but yrate-induced erythroid differentiation and reduced the action of Hemin; JNK i nhibitor SP600125 had not affected the differentiation by sodium butyrate but de creased the action of Hemin. Conclusion ERK positively regulat es Hemin-induced differentiation and negatively regulates the action of Sodium butyrate; meanwhile, the activation of JNK is required to induce erythroid diffe rentiation by Hemin not sodium butyrate in K562 cells.
出处 《中国药理学通报》 CAS CSCD 北大核心 2004年第11期1261-1264,共4页 Chinese Pharmacological Bulletin
基金 辽宁省自然科学基金资助项目 No 962 3 0 3 辽宁省教育厅基金资助项目 No 2 0 12 2 15 2
关键词 丁酸钠 氯高铁血红素 分化 ERK JNK P38 sodium butyrate Hemin erythroid differentiation ERK JNK p38
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