恒磁场对血管紧张素Ⅱ作用下人脐静脉内皮细胞增殖与凋亡的影响

Effects of constant magnetic field on proliferation and apoptosis of human umbilical vein endothelial cells intervened by angiotensin Ⅱ

目的 观察不同强度恒磁场对血管紧张素Ⅱ(AngⅡ)作用下人脐静脉内皮细胞 (HUVEC)增殖与凋亡的影响。方法 采用体外培养的第 3代HUVEC ,分为 6组 ,即对照组、AngⅡ组及AngⅡ +不同强度 (1× 10 -4T、5× 10 -4T、10× 10 -4T和 2 0× 10 -4T)恒磁场组。各组细胞于无磁场条件下培养或不同强度磁场作用 48h后收集标本 ,用MTT比色法和3 H TdR掺入法测定细胞增殖情况 ,末端脱氧核糖核酸酶介导的dUTP末端标记法(TUNEL法 )和流式细胞仪碘化丙啶染色法检测细胞凋亡情况。结果 1μmol/LAngⅡ可抑制HUVEC增殖 ,诱导HUVEC凋亡。AngⅡ +不同强度恒磁场组细胞增殖均显著高于AngⅡ组 (P <0 .0 5 ) ,细胞凋亡显著低于AngⅡ组 (P <0 .0 5 ) ,并呈现强度依赖效应。结论 1μmol/L AngⅡ可抑制HUVEC增殖并诱导HUVEC凋亡 ;(1～ 2 0 )× 10 -4T的恒磁场可强度依赖性拮抗AngⅡ对HUVEC的作用 ,促进HUVEC增殖并抑制HUVEC凋亡。

Objective To investigate the effects of constant magnetic field (CMF) on proliferation and apoptosis of human umbilical vein endothelial cells (HUVEC) in the presence of angiotensin Ⅱ (AngⅡ). Methods The third passage of cultured HUVEC was used. The cells were divided into six groups: control group, AngⅡ group, AngⅡ plus various intensities of constant magnetic field (i.e., 1×10 -4T,5×10 -4T,10×10 -4T and 20×10 -4T )group. The cell samples were collected at 48 hours later. Cell proliferation was measured by MTT chromatometry and 3H-TdR incorporation method. Apoptosis was determined by pyridine iodide staining on flow cytometry and tagged deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL). Results AngⅡ of the concentration of 1μmol/L inhibited proliferation of and induced apoptosis of HUVEC as compared with the control group(P<0.05). As far as the various intensities of constant magnetic field were concerned, proliferation of cells was significantly higher, while the apoptosis of cells was significantly lower when compared with those of the AngⅡ group (P<0.05), and a intensity-dependence effect was demonstrated. Conclusion AngⅡ of the concentration of 1μmol/L could inhibit proliferation of and induce apoptosis of HUVEC. Various intensities of constant magnetic field as used in this study showed antagonizing effects to that of AngⅡ on HUVEC, causing increased proliferation and decreased apoptosis of HUVEC.