CAJ | 학술논문

目的：探讨姜黄素对 CD34+CD38-KG1a 细胞增殖和凋亡的影响以及姜黄素联合白消安对 CD34+CD38-KG1a细胞的协同效应。方法流式细胞术检测细胞 CD34、CD38表面抗原的表达情况、姜黄素诱导 CD34+CD38-KG1a细胞的凋亡情况及其对CD34+CD38-KG1a细胞周期的影响。MTT法检测姜黄素对CD34+CD38-KG1a的增殖抑制作用及其与白消安联合作用的效应。甲基纤维素克隆形成实验检测细胞克隆形成能力。倒置光学显微镜观察细胞凋亡形态。Western blot检测Bcl-2蛋白表达水平。结果 KG1a 细胞株中 CD34+CD38-KG1a 细胞占(98.2±3.2)%。姜黄素对CD34+CD38-KG1a细胞具有增殖抑制作用,呈时间-剂量依赖性,并能降低 CD34+CD38-KG1a细胞的克隆形成能力。姜黄素与白消安相互作用系数(CDI)<1。CD34+CD38-KG1a 细胞被姜黄素阻滞于 G0/G1期,S期细胞明显减少,并能诱导CD34+CD38-KG1a 细胞凋亡。凋亡细胞体积变大,细胞结构不清,胞膜边缘粗糙。姜黄素能下调CD34+CD38-KG1a细胞Bcl-2蛋白表达水平。结论姜黄素通过降低细胞克隆形成能力、阻滞细胞于G0/G1期和诱导细胞凋亡,抑制CD34+CD38-KG1a细胞的增殖,姜黄素与白消安具有协同作用。Bcl-2蛋白表达水平下调可能促使姜黄素诱导CD34+CD38-KG1a细胞凋亡。
목적：탐토강황소대 CD34+CD38-KG1a 세포증식화조망적영향이급강황소연합백소안대 CD34+CD38-KG1a세포적협동효응。방법류식세포술검측세포 CD34、CD38표면항원적표체정황、강황소유도 CD34+CD38-KG1a세포적조망정황급기대CD34+CD38-KG1a세포주기적영향。MTT법검측강황소대CD34+CD38-KG1a적증식억제작용급기여백소안연합작용적효응。갑기섬유소극륭형성실험검측세포극륭형성능력。도치광학현미경관찰세포조망형태。Western blot검측Bcl-2단백표체수평。결과 KG1a 세포주중 CD34+CD38-KG1a 세포점(98.2±3.2)%。강황소대CD34+CD38-KG1a세포구유증식억제작용,정시간-제량의뢰성,병능강저 CD34+CD38-KG1a세포적극륭형성능력。강황소여백소안상호작용계수(CDI)<1。CD34+CD38-KG1a 세포피강황소조체우 G0/G1기,S기세포명현감소,병능유도CD34+CD38-KG1a 세포조망。조망세포체적변대,세포결구불청,포막변연조조。강황소능하조CD34+CD38-KG1a세포Bcl-2단백표체수평。결론강황소통과강저세포극륭형성능력、조체세포우G0/G1기화유도세포조망,억제CD34+CD38-KG1a세포적증식,강황소여백소안구유협동작용。Bcl-2단백표체수평하조가능촉사강황소유도CD34+CD38-KG1a세포조망。
Objective To investigate the effects of curcumin on proliferation and apoptosis of CD34+CD38-KG1a cells and its synergetic effect with busulfan on CD34+CD38-KG1a cells.Methods The expressions of CD34 and CD38 on the surface of KG1a cells and the effect of curcumin on the cell cycle and apoptosis in CD34+CD38-KG1a cells were detected by flow cytometry.MTT assay was used to analyze curcumin’s inhibitory effects on proliferation and synergistic effect with busulfan on CD34+CD38-KG1a.Clone formation rate was measured by methylcellulose colony-formation assay.Morphological changes of apoptotic cells were observed with the inverted optical microscope.The expression of Bcl-2 at the protein level was detected by Western blot.Results The percentage of CD34+CD38-KG1a was (98.2±3.2)% in KG1a cells.Curcumin could inhibit the proliferation in time-and dose-dependent manners and reduce the colony-formation ability of CD34+CD38-KG1a.The coefficient of drug interaction between curcumin and busulfan was less than 1.CD34+CD38-KG1a cells were arrested in the G0/G1 phase by decreasing S phase cells.Meanwhile,curcumin induced the apoptosis of CD34+CD38-KG1a cells. Apoptotic cells became bigger than normal ones,with unclear cell structure and rough edge of cell membrane.The expression of Bcl-2 at the protein level was down-regulated by curcumin.Conclusion Curcumin inhibited the proliferation of CD34+CD38-KG1a cells by reducing colony-formation ability,arresting cells in the G0/G1 phase and inducing apoptosis.Besides,there was a synergistic effect between curcumin and busulfan in CD34+CD38-KG1a cells.The down-regulated expression of Bcl-2 at the protein level may be associated with curcumin-induced apoptosis of CD34+CD38-KG1a cells.