【摘要】 目的:探讨维生素K₂对大鼠血管钙化形成及氧化应激损伤的作用。方法:24只大鼠随机分为4组:对照组、6周钙化组、12周钙化组和6周钙化+6周维生素K₂组。采用华法林诱导大鼠体内血管钙化形成。分别通过茜素红S染包法和邻甲酚肽络合酮比包法检测4组大鼠主动脉组织钙结节形成情况及钙沉积含量;活性氧检测试剂盒（二氢乙啶）检测大鼠主动脉组织活性氧阳性细胞数;透射电子显微镜检测大鼠血管平滑肌细胞线粒体形态变化。结果:6周及12周两个钙化组大鼠主动脉有钙结节形成,钙沉积含量及活性氧水平均显著高于对照组（P均<0.01）;6周钙化+6周维生素K₂组大鼠与两个钙化组相比,上述各指标均显著降低,差异均有统计学意义（P均<0.01）。两个钙化组大鼠血管平滑肌细胞线粒体肿胀,结构模糊不清,胞质内空泡变性;6周钙化+6周维生素K₂组大鼠血管平滑肌细胞体积与对照组比较无明显变化,胞质内未见空泡变性。结论:华法林诱导血管钙化形成与氧化应激损伤有关,氧化应激损伤可造成细胞超微结构损伤。维生素K₂可能通过减轻血管平滑肌细胞氧化应激损伤,改善血管钙化。更多还原

【Abstract】 Objective:To explore the effects of Vitamin K₂（VK₂） on theaortic artery calcification and oxidative stress injury in experimental rats.Methods:A total of 24 rats were divided into 4 groups:①Control group,②6-week calcification group,③ 12-week calcification group and ④6-week calcification + 6-week VK₂ group;n=6 in each group.The arterial calcification was induced by warfarin（WFN） treatment.The calcium nodule and deposition in rat’s theaortic artery were detected by Alizarin red staining and o-cresolphthalein complexone method,the reactive oxygen species（ROS） were measured by DHE probe staining and the morphological changes of mitochondria in smooth muscle cells were detected by transmission electron microscopy.Results:Calcification nodule formed in both 6-week and 12-week calcification groups,the calcification deposition and ROS were higher than Control group,P<0.01.Compared with both calcification groups,the above indexes were decreased in 6-week calcification + 6-week VK₂ group,P<0.01.Both calcification groups showed mitochondria swelling with unclear structure and cytoplasm vacuoles degeneration in vascular smooth muscle cells.The vascular smooth muscle cell volumes were similar between Control group and 6-week calcification + 6-week VK₂ group,and no cytoplasm vacuoles degeneration was observed.Conclusion:Warfarin induced aortic calcification is related to oxidative stress injury which may cause the ultramicro structural damage in smooth muscle cells;VK₂ may reduce the oxidative stress injury and improve the condition of vessel calcification in experimental rats.更多还原