CAJ | 학술논문

目的：研究血管紧张素Ⅱ（AngⅡ）对白血病 HL－60骨桥蛋白表达的影响及机制。方法：体外培养HL－60细胞株，予 AngII （终浓度10－9、10－8、10－7、10－6 mol／L ）刺激24 h 或予 AngⅡ（终浓度10－7 mol／L ）刺激12 h、24 h、48 h；先经 PI3K／AKT 抑制剂 LY294002（40 umol／L）预处理1 h，再予10－7 mol／L AngII 刺激24 h，收集细胞，采用western－blot 法检测OPN表达情况。结果：AngⅡ促进HL－60细胞表达OPN ，在一定浓度及时间内，其表达量随着AngⅡ浓度和时间的增加而增加，呈剂量和时间依赖性关系；经 LY294002预处理再予 AngⅡ刺激的HL－60细胞，与对照组比较，OPN表达明显抑制（P＜0．05）。结论：AngⅡ经PI3K／AKT信号通路诱导OPN的表达。
목적：연구혈관긴장소Ⅱ（AngⅡ）대백혈병 HL－60골교단백표체적영향급궤제。방법：체외배양HL－60세포주，여 AngII （종농도10－9、10－8、10－7、10－6 mol／L ）자격24 h 혹여 AngⅡ（종농도10－7 mol／L ）자격12 h、24 h、48 h；선경 PI3K／AKT 억제제 LY294002（40 umol／L）예처리1 h，재여10－7 mol／L AngII 자격24 h，수집세포，채용western－blot 법검측OPN표체정황。결과：AngⅡ촉진HL－60세포표체OPN ，재일정농도급시간내，기표체량수착AngⅡ농도화시간적증가이증가，정제량화시간의뢰성관계；경 LY294002예처리재여 AngⅡ자격적HL－60세포，여대조조비교，OPN표체명현억제（P＜0．05）。결론：AngⅡ경PI3K／AKT신호통로유도OPN적표체。
Objective: To investigate the effect and mechanism of antagonism Ⅱ (AngⅡ) on expression of osteopontin(OPN)in leukemic cell line HL-60. Methods: Leukemic cell line HL-60 was cultured in RPMI 1640 and stimulated by AngⅡ at the final concentration of 10-9,10-8,10-7,10-6 mol/L for 24 h or at final concentration of 10-7 mol/L for 12 h,24 h and 4 8h. HL-60 cells were pretreated with LY294002,a specific inhibitor of PI3K/AKT signaling pathway,at final concentration of 40 umol/L for 1h,followed by incubation with AngⅡ at final concentration of 10-7mol/L for 24h.The cells were collected. The expression of OPN was detected by Western blotting. Results:In HL-60 cells,the expression of OPN was apparently elevated when incubated with AngⅡ.With the increase in AngⅡconcentration or the extension of incubation hours,the expression of OPN was increasd gradually in a dose- and time-dependent manner. HL-60 cells pretreated with LY294002 and incubated with had a significant decrease in the OPN expression as compared with control group (P<0.05). Conclusion:The expression of OPN in AngⅡ-induced HL-60 cells is regulated by the PI3K/AKT signaling pathway.