CAJ | 학술논문

目的：探讨血管紧张素Ⅱ1型受体（AT1R）拮抗剂氯沙坦抑制血管紧张素Ⅱ（AngⅡ）介导的原代急性髓系白血病（AML）细胞的增殖作用及机制。方法：MTT法观察Ang Ⅱ对原代AML细胞、正常骨髓单个核细胞增殖的影响以及氯沙坦和 AT2R拮抗剂PD123319对Ang II促原代AML细胞增殖的拮抗作用；Elisa 法检测氯沙坦对血管紧张素II作用下原代AML分泌MMP-9的影响。结果：AngII 能剂量和时间依赖性促进原代 AML 细胞增殖（P ＜0．05），而对正常骨髓无此作用；氯沙坦随浓度和时间依赖性阻断 AngII 作用下白血病细胞增殖（P ＜0．05）；氯沙坦能明显下调AngII增加原代AML细胞MMP-9的分泌（P ＜0．05）。结论：氯沙坦通过抑制MMP-9分泌阻断AngII/AT1R介导的白血病细胞增殖。
목적：탐토혈관긴장소Ⅱ1형수체（AT1R）길항제록사탄억제혈관긴장소Ⅱ（AngⅡ）개도적원대급성수계백혈병（AML）세포적증식작용급궤제。방법：MTT법관찰Ang Ⅱ대원대AML세포、정상골수단개핵세포증식적영향이급록사탄화 AT2R길항제PD123319대Ang II촉원대AML세포증식적길항작용；Elisa 법검측록사탄대혈관긴장소II작용하원대AML분비MMP-9적영향。결과：AngII 능제량화시간의뢰성촉진원대 AML 세포증식（P ＜0．05），이대정상골수무차작용；록사탄수농도화시간의뢰성조단 AngII 작용하백혈병세포증식（P ＜0．05）；록사탄능명현하조AngII증가원대AML세포MMP-9적분비（P ＜0．05）。결론：록사탄통과억제MMP-9분비조단AngII/AT1R개도적백혈병세포증식。
To explore the antagonistic effect and mechanism of Losartan on Angiotensin (AngII)-induced proliferation of primary acute myeloid leukemia (AML)cells. Methods:MTT assay was used to observe the proliferation effect of AngII on primary AML cells and normal bone marrow mononuclear cells,and the antagonistic effects of Losartan [an antagonist of angiotensin II type 1 receptor (AT1R)] and PD123319 (an antagonist of AT2R) were also observed.MMP-9 was detected by Elisa when the cells were treated with Losartan. Results: Compared with the control cells,AngII significantly increased the proliferation of AML cells in a dose- dependent and time-dependent manner(P<0.05).AngII did not stimulate the proliferation of normal bone marrow mononuclear cells. The proliferative effect of AngII was effectively blocked by the AT1R blocker Losartan (P<0.05).Losartan significantly reduced the secretion of MMP-9 promoted by AngII on primary AML cells (P<0.05). Conclusions: Losartan effectively inhibits AngII-induced proliferation of primary AML cells by decreased the secretion of MMP-9.