雷公藤甲素通过MDM2-p53通路诱导白血病K562／G01细胞凋亡的研究  

Mechanisms of MDM2-p53 pathway in apoptosis of in K562/G01 cells induced by triptolide

作　　者：焦晓琳 马粱明 鹿育晋[2] 

机构地区：[1]山西医科大学研究生学院,太原030001 [2]山西医学科学院山西大医院血液科,太原030032

出　　处：《白血病．淋巴瘤》2016年第6期336-339,345,共5页Journal of Leukemia & Lymphoma

摘　　要：目的探讨雷公藤甲素（TP）诱导伊马替尼耐药的K562／G01细胞的凋亡作用及机制。方法采用四甲基偶氮唑盐（MTr）法测定不同浓度TP作用的K562／G01细胞增殖抑制情况，流式细胞术检测细胞凋亡率，实时荧光定量PCR法检测bcr-abl、XIAP、MDM2、p53等mRNA的表达。结果10、20、40、80、100nmol／LTP作用12、24、48h，K562／G01细胞增殖受到抑制，呈时间．剂量依赖性；20、40nmol／LTP分别作用K562／G01细胞12h和24h，细胞凋亡率呈时间．剂量依赖性；TP能降低ber-abl、XIAP、MDM2mRNA的表达，升高p53mRNA的表达。结论TP可抑制K562／G01细胞增殖，诱导凋亡，其机制可能是通过XIAP．MDM2-p53通路相关基因的表达影响K562／G01细胞的增殖及凋亡。Objective To explore the apoptosis of K562/G01 cells induced by triptolide through MDM2/p53 signaling pathway. Methods K562/G01 cell line was treated with different concentrations of triptolide. MTT was used to detect the cell proliferation inhibition rate. FCM was used to determine the apoptosis rate changes in 12 h and 24 h. The mRNA expression levels of bcr-abl, XIAP, MDM2, p53 were detected by real-time quantitative PCR. Results After treatment by 10, 20, 40, 80, 100 nmol/L TP in 12, 24, 48 h, the viability of K562/G01 cells was inhibited in time-dose dependence manner. K562/G01 cells was treated by 20 nmol/L, 40 nmol/L TP after 12 h, 24 h, the cell apoptosis rate was rising with drug concentration and time. The bcr-abl, XIAP, MDM2 mRNA expression was down-regulated and p53 mRNA expression was up-regulated by TP. Conclusion TP can inhibit the growth of K562/G01 cell line and induce apoptosis through XIAP-MDM2-p53 signaling pathway.

关 键 词：白血病 雷公藤甲素 K562iG01细胞 MDM2 P53 XIAP 细胞凋亡 

分 类 号：R285[医药卫生—中药学]