摘要
目的:观察和厚朴酚是否增强NK-92细胞对人急性髓细胞白血病KG-1a细胞的杀伤作用,并探讨其机制。方法:CCK8法检测和厚朴酚对KG-1a细胞的毒性作用,乳酸脱氢酶(lactate dehydrogenase,LDH)法检测NK-92细胞对KG-1a细胞的杀伤作用,流式细胞术检测和厚朴酚对KG-1a细胞凋亡的影响以及KG-1a细胞表面自然杀伤细胞2族成员D(natural killer group 2,member D,NKG2D)配体ULBP1、ULBP2和ULBP3的表达。结果:CCK8实验结果显示,随着和厚朴酚浓度的增高,KG-1a细胞的活力逐渐降低,但24 h后KG-1a细胞活力仍大于40%。LDH实验表明,10μmol/L的和厚朴酚处理KG-1a细胞24 h后,NK-92细胞对KG-1a细胞的杀伤率比用药前显著提高(P<0.01)。流式细胞术结果证实,和厚朴酚处理24 h后,在效靶比为5∶1时,NK-92细胞诱导KG-1a细胞的凋亡率显著高于未处理组(P<0.01)。同时,KG-1a细胞表面NKG2D配体(ULBP1、ULBP2和ULBP3)的表达显著高于未处理组(P<0.05)。结论:和厚朴酚可以通过上调KG-1a细胞表面NKG2D配体的表达增强NK-92细胞对KG-1a细胞的杀伤作用。
AIM:To investigate the mechanisms of honokiol enhancing the killing effect of NK-92 cells on human acute myeloid leukemia KG-1a cells.METHODS:The CCK8 assay was used to detect the toxic effect of honokiol on KG-1a cells.The killing effect of NK-92 cells on KG-1a cells was detected by lactate dehydrogenase(LDH)assay.Flow cytometry was used to detect KG-1a cell apoptosis and expression levels of natural killer group 2 member D(NKG2D)ligands,ULBP1,ULBP2 and ULBP3,on the surface of KG-1a cells before and after honokiol treatment.RESULTS:The results of CCK8 assay showed that as the concentration of honokiol increased,the viability of KG-1a cells gradually decreased,but still greater than 40%after honokiol treatment for 24 h.The LDH assay showed that the killing rate of NK-92 cells to KG-1a cells was significantly increased after treatment with 10μmol/L honokiol for 24 h(P<0.05).Flow cytometry results showed that the apoptosis rate of KG-1a cells induced by NK-92 cells in honokiol treatment group was significantly higher than that in non-treatment group when the effector-to-target cell ratio was 5∶1(P<0.01).Meanwhile,the ex‐pression levels of NKG2D ligands(ULBP1,ULBP2 and ULBP3)on the surface of KG-1a cells in honokiol treatment group were significantly higher than those in non-treatment group(P<0.05).CONCLUSION:Honokiol enhances the killing effect of NK-92 cells on KG-1a cells by up-regulating the expression of NKG2D ligands on the surface of KG-1a cells.
作者
张海鹏
陈景
陈秀云
叶汉深
李军
张普山
佘妙容
李晓红
ZHANG Hai-peng;CHEN Jing;CHEN Xiu-yun;Ye Han-sen;Li Jun;ZHANG Pushan;She miao-rong;Li xiao-hong(Department of Blood Transfusion,Guangdong Provincial People's Hospital,Guangdong Academy of Medical Sciences,Guangdong Academy of Medical Sciences,Guangzhou 510080,China;Guangdong Provincial Key laboratory of South China Structural Heart disease,Guangdong Cardiovascular Institute,Guangdong Academy of Medical Sciences,Guangzhou 510080,China;Medi-cal Research Center,Guangdong Provincial People's Hospital,Guangdong Academy of Medical Sciences,Guangdong Academy of Medical Sciences,Guangzhou 510080,China;Department of Hematology,Guangdong Provincial People's Hospital,Guangdong Academy of Medical Sciences,Guangzhou 510080,China)
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2021年第3期475-480,共6页
Chinese Journal of Pathophysiology
基金
广东省中医药局科研项目(No.20191003)。
