| 和厚朴酚对HL-60细胞增殖抑制作用及其相关机制研究 |
| |
| 引用本文： | 范佳鑫,;曾英坚,;翁光样,;吴建伟,;李章球,;李元明,;郑荣,;郭坤元. 和厚朴酚对HL-60细胞增殖抑制作用及其相关机制研究[J]. 中国实验血液学杂志, 2014, 0(6): 1577-1583 |
| |
| 作者姓名： | 范佳鑫, 曾英坚, 翁光样, 吴建伟, 李章球, 李元明, 郑荣, 郭坤元 |
| |
| 作者单位： | [1]江门市五邑中医院/暨南大学附属江门中医院血液科,广东江门529000; [2]南方医科大学珠江医院血液科,广东广州510282 |
| |
| 摘 要： | 本研究旨在探讨和厚朴酚（honokiol,HNK）对急性髓系白血病细胞HL-60增殖和凋亡的影响及其作用机制。MTT法检测HNK对HL-60细胞增殖抑制作用。流式细胞术检测细胞周期变化。Annexin V/PI法检测细胞凋亡情况。Western blot检测细胞周期蛋白（cyclins）、细胞周期蛋白依赖性激酶（CDK）、P53、P21、P27、BCL-2、BCLXL、BAX、caspase-3、-9、M APK信号通路蛋白。结果表明：HNK能够抑制HL-60细胞增殖,呈时间剂量依赖性。HNK阻滞HL-60细胞于G0/G1期,S期细胞显著减少（P〈0.05）。HNK作用HL-60细胞24 h后,cyclin D1、cyclin A、cyclin E、CDK2、4、6表达显著下调（P〈0.05）,P53、P21表达显著上调（P〈0.05）。HNK作用24 h后HL-60细胞凋亡增加,活化的caspase-3、-9表达显著增加;BCL-2和BCL-XL表达下调,而BAX表达上调。MAPK亚族P38、JNK表达无明显变化;而M EK1/2-ERK1/2的表达显著下调（P〈0.05）。结论：HNK通过干预M EK1/2-ERK1/2信号通路阻滞HL-60细胞于G0/G1期并诱导HL-60细胞凋亡。
|
| 关 键 词： | 和厚朴酚 HL-60细胞 白血病 凋亡 细胞周期 |
Effect of Honokiol on Proliferation and Apoptosis in HL-60 Cells and Its Potential Mechanism |
| |
| Affiliation: | FAN Jia-Xin, ZENG Ying-Jian , WENG Guang-Yang , WU Jian-Wei, LI Zhang-Qiu, LI Yuan-Ming, ,ZHENG Rong, GUO Kun-Yuan( 1 Department of Hematology, Wuyi Hospital of Traditional Chinese Medicine/Traditional Chinese Medicine Hospital of Jinan University Medical College, Jiangmen 529000, Guangdong Province, China ; 2 Department of Hematology, Zhufiang Hospital, Southern Medical University, Guangzhou 510282, Guangdong Province, China) |
| |
| Abstract: | This study was aimed to investigate the effect of Honokiol（HNK）on proliferation and apoptosis of acute myeloid leukemia HL-60 cells and its potential mechanism.Inhibitory effect of HNK on the HL-60 cell proliferation was detected by MTT assay.Flow cytometry was used to detect the change of cell cycle and AnnexinV /PI staining was used to detect apoptosis.Western blot was applied to analyze the cell cycle protein（ cyclins）,cyclin-dependent kinase（ CDK）,P53P21P27BCL-2BCL-XLBaxcaspase-3 /9 and proteins for MAPK signal pathway.The results showed that HNK could inhibit the proliferation of HL-60 cells in time-and dose dependent ways.HNK arrested HL-60 cells in G/Gphaseand S phase cells decreased significantly（ P〈0.05）.The expression of cyclin D1 cyclin Acyclin E and CDK2 /4 /6 were significantly down-regulated（P〈0.05）,the expression of P53 and P21 was significantly upregulated after treating for 24 h with HNK（ P〈0.05）.After 24 h treatment with HNKHL-60 cell apoptosis increased significantly with the upregulation of activated caspase-39 BAX expression and the downregulation of BCL-2BCL-XL expression.The MAPK subfamilyP38 and JNK were not significantly changedbut the expression of MEK1 /2- ERK1 /2 was significantly downregulated（P〈0.05）.It is concluded that HNK arrestes the cells at G/Gphase and induces HL-60 cell apoptosis through the intervention of MEK1 /2- ERK1 /2 signaling pathway. |
| |
| Keywords: | honokiol HL-60 cell leukemia apoptosis cell cycle |
| 本文献已被 维普 等数据库收录！ |
|
