miR-203提高白血病K562细胞对熊果酸的敏感性研究  

Enhanced sensitivty of leukemic K562 cell to ursolic acid by miR-203

作　　者：黄之虎[1] 农朝赞[1] 农少云[1] 郭凌霄[1] 李育敏[1] 何金花 韦仕喻[1] 

机构地区：[1]广西壮族自治区民族医院检验科,广西南宁530001 [2]广东省广州市番禺区中心医院检验科,广东广州511400

出　　处：《中国药理学通报》2014年第7期969-972,共4页Chinese Pharmacological Bulletin

基　　金：广西自然科学基金资助项目(No 2012GXNSFAA053177);广西壮族自治区中医药管理局中医药科技专项(GZKZ1136)

摘　　要：目的研究miR-203影响白血病K562细胞对熊果酸的敏感性及可能的作用机制。方法利用脂质体LipofectamineTM2000将miR-203的真核表达载体PmiR-203转染K562细胞。MTT法检测单纯使用PmiR-203、熊果酸以及两者联合使用对细胞的增殖抑制作用;Annexin V/PI双染法检测细胞早期凋亡率;Western blot检测细胞内bcr/abl蛋白表达水平。结果熊果酸与PmiR-203联合使用后,IC50从44.3μmol·L-1降低到30.7μmol·L-1,敏感性提高到单纯使用熊果酸的1.55倍。PmiR-203联合熊果酸组细胞早期凋亡率明显增加(P<0.05)。PmiR-203组细胞内bcr/abl的表达水平明显降低。结论PmiR-203可通过抑制Bcr/abl融合基因的表达发挥抗白血病作用,与熊果酸联合使用可提高白血病K562细胞对熊果酸的敏感性。Aim To study the influences of miR-203 on ursolic acid （UA ） sensitivity in leukemic K562 cell.Methods In the experimental system,eukaryot-ic expression vector of hsa-miR-203 （PmiR-203 ）was transfected into K562 cells using LipofectamineTM 2000.K562 cells were incubated with different con-centration of UA alone or in combination with PmiR-203 .The cell proliferation was analyzed by MTT as-say.The cell apoptosis was measured by double stai-ning with Annexin V and Propidium Iodide.The ex-pression of Bcr/abl protein was detected by Western Blot.Results The miR-203 promoted the sensitivity＆amp;nbsp;of UA by up to 1 .55-fold and the IC50 was reduced from 44.3μmol · L-1 to 30.7 μmol · L-1 .The a-mount of apoptotic cells was increased in UA combined with PmiR-203 group （P＆lt;0.05）.PmiR-203 downreg-ulated the expression of Bcr/abl protein in K562 cells. Conclusion Our results support a substantial role of miR-203 that enhances UA sensitivity in K562 cell and the mechanism appears to be related to the dounregula-tion of Bcr/abl by miR-203 .

关 键 词：miR-203 熊果酸 白血病K562细胞 BCR ABL 增殖 凋亡 

分 类 号：R284.1[医药卫生—中药学] R329.24[医药卫生—中医学]