中国临床药理学杂志
中國臨床藥理學雜誌
중국림상약이학잡지
The Chinese Journal of Clinical Pharmacology
2015年
17期
1757-1759,1785
,共4页
邵燕萍%罗文达%郭群依%蔡真
邵燕萍%囉文達%郭群依%蔡真
소연평%라문체%곽군의%채진
多发性骨髓瘤%雷公藤内酯醇%KM3%组蛋白3 第4位赖氨酸的三甲基化%增殖%凋亡
多髮性骨髓瘤%雷公籐內酯醇%KM3%組蛋白3 第4位賴氨痠的三甲基化%增殖%凋亡
다발성골수류%뢰공등내지순%KM3%조단백3 제4위뢰안산적삼갑기화%증식%조망
multiple myeloma%triptolide%KM3%H3K4me3%proliferation%apoptosis
目的：探讨雷公藤内酯醇对多发性骨髓瘤KM3细胞增殖、凋亡和组蛋白3第4位赖氨酸的三甲基化（ H3 K4 me3）蛋白表达的影响。方法以人多发性骨髓瘤细胞株 KM3为研究对象，用噻唑蓝（ MTT ）法检测细胞增殖活性；Annexin V－FITC／PI双标流式细胞术和共聚焦显微镜检测细胞凋亡；蛋白质印迹法和共聚焦显微镜检测雷公藤内酯醇对KM3细胞H3K4me3表达的影响。结果雷公藤内酯醇对KM3细胞的增殖有明显抑制作用，呈现剂量和时间依赖关系（ P＜0.05）。雷公藤内酯醇对KM3细胞有明显诱导凋亡的作用，并且随着雷公藤内酯醇作用浓度的增加，细胞凋亡比例逐渐增加，其中总凋亡率分别为（48.97±1.78）％，（53.72±2.21）％和（60.75±2.43）％。 H3K4me3集中分布于细胞核内，80 nmol· L－1雷公藤内酯醇干预48 h后，KM3细胞H3K4me3的平均荧光强度值（21.96±0.34）显著低于对照组（39.86±0.47）（ P ＜0.05）。结论雷公藤内酯醇可抑制多发性骨髓瘤KM3细胞增殖，诱导KM3细胞凋亡，降低H3K4me3蛋白表达。
目的：探討雷公籐內酯醇對多髮性骨髓瘤KM3細胞增殖、凋亡和組蛋白3第4位賴氨痠的三甲基化（ H3 K4 me3）蛋白錶達的影響。方法以人多髮性骨髓瘤細胞株 KM3為研究對象，用噻唑藍（ MTT ）法檢測細胞增殖活性；Annexin V－FITC／PI雙標流式細胞術和共聚焦顯微鏡檢測細胞凋亡；蛋白質印跡法和共聚焦顯微鏡檢測雷公籐內酯醇對KM3細胞H3K4me3錶達的影響。結果雷公籐內酯醇對KM3細胞的增殖有明顯抑製作用，呈現劑量和時間依賴關繫（ P＜0.05）。雷公籐內酯醇對KM3細胞有明顯誘導凋亡的作用，併且隨著雷公籐內酯醇作用濃度的增加，細胞凋亡比例逐漸增加，其中總凋亡率分彆為（48.97±1.78）％，（53.72±2.21）％和（60.75±2.43）％。 H3K4me3集中分佈于細胞覈內，80 nmol· L－1雷公籐內酯醇榦預48 h後，KM3細胞H3K4me3的平均熒光彊度值（21.96±0.34）顯著低于對照組（39.86±0.47）（ P ＜0.05）。結論雷公籐內酯醇可抑製多髮性骨髓瘤KM3細胞增殖，誘導KM3細胞凋亡，降低H3K4me3蛋白錶達。
목적：탐토뢰공등내지순대다발성골수류KM3세포증식、조망화조단백3제4위뢰안산적삼갑기화（ H3 K4 me3）단백표체적영향。방법이인다발성골수류세포주 KM3위연구대상，용새서람（ MTT ）법검측세포증식활성；Annexin V－FITC／PI쌍표류식세포술화공취초현미경검측세포조망；단백질인적법화공취초현미경검측뢰공등내지순대KM3세포H3K4me3표체적영향。결과뢰공등내지순대KM3세포적증식유명현억제작용，정현제량화시간의뢰관계（ P＜0.05）。뢰공등내지순대KM3세포유명현유도조망적작용，병차수착뢰공등내지순작용농도적증가，세포조망비례축점증가，기중총조망솔분별위（48.97±1.78）％，（53.72±2.21）％화（60.75±2.43）％。 H3K4me3집중분포우세포핵내，80 nmol· L－1뢰공등내지순간예48 h후，KM3세포H3K4me3적평균형광강도치（21.96±0.34）현저저우대조조（39.86±0.47）（ P ＜0.05）。결론뢰공등내지순가억제다발성골수류KM3세포증식，유도KM3세포조망，강저H3K4me3단백표체。
Objective To investigate the effect of triptolide on the proliferation, apoptosis and and H3K4me3 protein expression in multiple myeloma KM3 cell.Methods The MM KM3 cell line was cultured with triptolide.Cell proliferation was detected by MTT method .Apoptosis was evaluated by Annexin -V -FITC/PI -labeled flow cytometry and confocal microscopy.The expression of H3K4me3 in KM3cells was assayed by Western blotting and confocal microscopy.Results Triptolide had obvious inhibition on proliferation of KM 3 cells and showed a dose and time dependence.Triptolide had obvious inhibition on apoptosis of KM 3 cells,and with the increase of triptolide concentration , the apoptosis ratio increased gradually. The the total apoptosis rates were (48.97 ±1.78 )%, ( 53.72 ±2.21 )% and ( 60.75 ±2.43 )%.Confocal laser scanning microscopy showed H 3K4me3 accumulated in the nucleus, after 48 h intervention of 80 nmol· L-1 of triptolide, the mean value of fluorescence intensity of H3K4me3 in KM3 cells (21.96+0.34 ) was significantly lower than that in the control group ( 39.86 ±0.47 ) ( P <0.05 ) .Conclusion Triptolide inhibited cell proliferation, induced cell apoptosis, reduced the expression of H3K4me3 protein.
