摘要
目的探讨丹参酮ⅡA联合自然杀伤(NK)细胞对急性髓系白血病细胞杀伤作用的机制。方法采用浓度分别为0、8、16、32、64μmol/L的丹参酮ⅡA处理NK细胞和HL-60细胞,用噻唑蓝(MTT)实验检测细胞增殖变化。钙黄绿素-AM释放法检测杀伤率;酶联免疫吸附法(ELISA)法检测肿瘤坏死因子α(TNF-α)、干扰素γ(IFN-γ)含量;流式细胞术检测NKG2D配体MICA、MICB、ULBP1及ULBP2表达率。结果丹参酮ⅡA呈剂量效应抑制急性髓系白血病细胞增殖、促进NK细胞增殖,丹参酮ⅡA浓度为32μmol/L增殖率较高。丹参酮ⅡA+NK细胞组的杀伤率较丹参酮ⅡA组、NK细胞组明显增加。丹参酮ⅡA+NK细胞+HL-60细胞组的TNF-α、IFN-γ含量较丹参酮ⅡA+NK细胞组、NK细胞+HL-60细胞组、NK细胞组明显增加;丹参酮ⅡA+NK细胞、NK细胞+HL-60细胞组的TNF-α、IFN-γ含量较NK细胞组明显增加。丹参酮ⅡA+HL-60细胞组的NKG2D配体MICA、MICB、ULBP1、ULBP2表达率较HL-60细胞组明显增加。结论丹参酮ⅡA联合NK细胞对急性髓系白血病细胞具有杀伤作用,其作用机制可能与丹参酮ⅡA促进NK细胞中TNF-α、IFN-γ表达以及促进HL-60细胞中NKG2D配体表达有关。
To investigate the killing effects of tanshinoneⅡA combined with natural killer(NK)cells on acute myeloid leukemia cells,NK cells and HL-60 cells were treated with tanshinone IIA at concentrations of 0,8,16,32or 64μmol/L.The cell proliferation of HL-60 cells was detected by the thiazole blue(MTT)assay,while the killing rate was detected by calcein-AM release method;ELISA method was used to detect the levels of tumor necrosis factor alpha(TNF-α)and interferon gamma(IFN-γ);flow cytometry was used to detect the expression of NKG2D ligands MICA,MICB,ULBP1,ULBP2.Data showed that tanshinone IIA could inhibit the proliferation of acute myeloid leukemia cells and promote the proliferation of NK cells both in a dose-effect manner,and tanshinone IIA at 32μmol/L demonstrated higher promoting effect on NK cell proliferation.The killing rate of tanshinoneⅡA+NK cell group was significantly higher than those of tanshinoneⅡA group and NK cell group.The levels of TNF-αand IFN-γin the tanshinoneⅡA+NK cell+HL-60 cell group were significantly higher than those in the tanshinoneⅡA+NK cell group,NK cell+HL-60 cell group,and NK cell group;the levels of TNF-αand IFN-γin tanshinone IIA+NK cell group and NK cell+HL-60 cell group were significantly higher than those in NK cell group.The expression of NKG2D ligands MICA,MICB,ULBP1 and ULBP2 in the tanshinoneⅡA+HL-60 cell group were significantly higher those in the HL-60 cell group.In conclusion,tanshinoneⅡA combined with NK cells can killing acute myeloid leukemia cells synergistically,and its mechanism may be related to promoting the expression of TNF-αand IFN-γin NK cells and the expression of NKG2D ligands in HL-60 cells.
作者
游崇登
陈聪杰
陈爱珍
马小美
YOU Chongdeng;CHEN Congjie;CHEN Aizhen;MA Xiaomei(Department of Blood,Longyan First Hospital Affiliated to Fujian Medical University,Longyan 364000,China)
出处
《免疫学杂志》
CAS
CSCD
北大核心
2022年第7期568-573,共6页
Immunological Journal
