恒磁场对大鼠主动脉平滑肌细胞基质金属蛋白酶的影响

Effect of constant magnetic field on matrix metalloproteinase of rat vascular smooth muscle cells

目的:观察不同磁感应强度恒磁场对培养的大鼠主动脉血管平滑肌细胞基质金属蛋白酶2活性的影响,以探讨磁场是否能用于经皮冠状动脉支架介入治疗术后再狭窄的防治。方法:实验于2005-12/2006-08在解放军第四军医大学西京医院心内科实验室完成。取纯种雄性SD大鼠,体质量200～250g,用含体积分数为0.1小牛血清的DMEM培养液体外培养大鼠主动脉血管平滑肌细胞,实验随机分为对照组,1Gs恒磁场组、5Gs恒磁场组、10Gs恒磁场组、50Gs恒磁场组,其中对照组不予磁场干预,其他各组分别给予磁场干预继续培养48h。运用基质金属蛋白酶2活性酶图分析法结合吸光度扫描分析,观察恒磁场对血管平滑肌细胞的基质金属蛋白酶2表达的影响。结果:与对照组相比,各组基质金属蛋白酶2的活性均明显被抑制,差异有显著性意义[(831.25±2.38)×102,(690.57±2.57)×102,(574.35±1.98)×102,(401.05±1.96)×102,(316.23±3.24)×102,P<0.05],不同磁场强度组组间分析显示具有剂量依赖性,随磁场强度加大,抑制作用也增强。结论:适当强度的恒磁场抑制血管平滑肌细胞的基质金属蛋白酶2活性的表达,磁场对经皮冠状动脉支架介入治疗术后的再狭窄可能具有防治作用。

AIM： To investigate the effect of constant magnetic field at different intensities on matrix metalloproteinase-2 （MMP-2） expression of rat vascular smooth muscle cell （VSMC） cultured in vitro, and observe if magnetic field can be used to treat the restenosis after percutaneous coronary intervention. METHODS： The experiment was carded out in the Laboratory of Cardiology, Xijing Hospital, the Fourth Military Medical University of Chinese PLA from December 2005 to August 2006. Purebred SD male rats of 200-250 g weight were adopted in this study, VSMCs were cultured in vitro with DMEM containing 0.1 volume fraction of calf serum. VSMCs were exposed for 48 hours under constant magnetic field of different intensities （1, 5, 10, 50 Gs）. The expression of MMP-2 influenced by constant magnetic field was monitored by image analysis and absorbance scanning. RESULTS： Compared with control group, the activity of MMP-2 was significantly inhibited in MMP-2 groups [（831.25± 2.38）×10^2, （690.57±2.57）×10^2, （574.35±1.98）×10^2, （401.05±1.96）×10^2, （316.23±3.24）×10^2, P 〈 0.05], and the inhibition exhibited a dose-dependent manner with the intensity of constant magnetic field. CONCLUSION： The expression of MMP-2 is significantly inhibited by constant magnetic field of appropriate intensity. Constant magnetic field has the possible preventive and curative effects for the restenosis after percutaneous coronary intervention.