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刘淑艳,黄畅,林圣云.白花蛇舌草提取物抗多发性骨髓瘤细胞的机制研究[J].浙江中西医结合杂志,2019,29(12):
白花蛇舌草提取物抗多发性骨髓瘤细胞的机制研究
The study of the Mechanism of Anti-multiple Myeloma cells by monomers of the extract of hedyotis diffusa
投稿时间:2019-06-04  修订日期:2019-10-12
DOI:
中文关键词:  多发性骨髓瘤、白花蛇舌草提取物、细胞周期、凋亡
英文关键词:MULTIPLE MYELOMA,HEDYOTIS DIFFUSA EXTRACTION(HDE),CELL CYCLE,APOPTOSIS
基金项目:浙江省自然科学基金青年基金项目(LQ15H080002);浙江省医药卫生科技计划平台骨干人才项目(2015RCA019)
作者单位E-mail
刘淑艳 浙江省中医院 catmi7903@163.com 
黄畅 浙江医院  
林圣云* 浙江省中医院 lsyww2012@163.com 
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中文摘要:
      目的 探讨白花蛇舌草提取物(HDE)抗多发性骨髓瘤细胞的机制。方法 观察50、100、150μg/mL HDE、2.5、5、10uM三氧化二砷(As2O3)及25、50、100nM硼替佐米(Bortezomib)浓度对骨髓瘤细胞株的增殖抑制,细胞周期及诱导凋亡的影响,明确白花蛇舌草中具有抗肿瘤作用的单体成分,同时讨论HDE抗肿瘤作用机制。结果 不同浓度As2O3、硼替佐米及HDE作用于RPMI 8226及NCI-H929细胞增殖的抑制作用具有浓度及时间依赖性;浓度增加了25ug/ml,抑制率增加50%,HDE浓度为50-75μg/mL对细胞的抑制作用最为明显。 100nM硼替佐米作用于RPMI 8226及NCI-H929 24h,分别使G2/M期升至为70.10%、73.99%,150μg/mLHDE作用于RPMI 8226及NCI-H929 24h,分别使G0/G1期升至为45.15%、36.28%,而10uM As2O3作用于NCI-H929 24h,使G0/G1期升至为40.59%;3种药物均可诱导细胞凋亡,150μg/mLHDE作用于RPMI 8226及NCI-H929 48h,凋亡率为14.44±0.50%、24.90±0.76%。结论 HDE在一定浓度范围内对多发性骨髓瘤细胞具有较为明显剂量依赖的杀伤作用,其中在浓度50~75μg/mL对细胞的抑制作用增加最为明显。HDE是通过诱导细胞凋亡及阻滞细胞周期来抑制骨髓瘤细胞增殖。
英文摘要:
      PURPOSE: Study on the mechanism of anti-mμLtiple myeloma cells by monomers of the extract of hedyotis diffusa. METHOD: To observe the effects of 50、100、150μg/mL HDE, 2.5、5、10uM As2O3 and 25、50、100nM Bortezomib on proliferation inhibition, cell cycle and apoptosis of RPMI 8226 and NCI-H929, and to clarify the anti-tumor monomer components of Hedyotis diffusa, and to discuss the anti-tumor mechanism of HDE. RESΜLTS: The inhibitory effects of HDE,As2O3 and Bortezomib on the proliferation of RPMI 8226 and NCI-H929 cells were concentration-and time-dependent. The concentration increased by 25ug/ml and the inhibition rate increased by 50%,50-75 μg/mL HDE has the most obvious inhibitory effect on cells. 100nM bortezomib was applied to RPMI 8226 and NCI-H929 for 24h, G2/M phase was increased to 70.10% and 73.99%, 150μg/mL HDE was applied to RPMI 8226 and NCI-H929 for 24h, G0/G1 was increased to 45.15% and 36.28%, While 10uM As2O3 acted on NCI-H929 for 24h, the G0/G1 was raised to 40.59%.All the three drμgs can promote apoptosis of RPMI 8226 andNCI-H929 cells, 150 μg/mL HDE was applied to RPMI 8226 and NCI-H929 for 48h, the apoptotic rate was 14.44±0.50% and 24.90±0.76%.. CONCLUSION :HDE has a dose-dependent killing effect on mμLtiple myeloma cells in a certain concentration range. The inhibitory effect on cells was the most obvious at the concentration of 50-75μg/mL. HDE inhibits the proliferation of myeloma cells by inducing apoptosis and blocking cell cycle. It turn out that the HDE inhibits proliferation of myeloma cells by promoting apoptosis and blocking the cell cycle.
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