CAJ | 학술논문

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染色法和邻甲酚肽络合酮比色法检测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。
목적：탐토유생소K2대대서혈관개화형성급양화응격손상적작용。 　　방법：24지대서수궤분위4조：대조조、6주개화조、12주개화조화6주개화+6주유생소K2조。채용화법림유도대서체내혈관개화형성。분별통과천소홍S염색법화린갑분태락합동비색법검측4조대서주동맥조직개결절형성정황급개침적함량；활성양검측시제합（이경을정）검측대서주동맥조직활성양양성세포수；투사전자현미경검측대서혈관평활기세포선립체형태변화。 　　결과：6주급12주량개개화조대서주동맥유개결절형성，개침적함량급활성양수평균현저고우대조조（P균<0.01）；6주개화+6주유생소K2조대서여량개개화조상비，상술각지표균현저강저，차이균유통계학의의（P균<0.01）。량개개화조대서혈관평활기세포선립체종창，결구모호불청，포질내공포변성；6주개화+6주유생소K2조대서혈관평활기세포체적여대조조비교무명현변화，포질내미견공포변성。 　　결론：화법림유도혈관개화형성여양화응격손상유관，양화응격손상가조성세포초미결구손상。유생소K2가능통과감경혈관평활기세포양화응격손상，개선혈관개화。
Objective: To explore the effects of Vitamin K2 (VK2) on theaortic artery calciifcation and oxidative stress injury in experimental rats. Methods: A total of 24 rats were divided into 4 groups:①Control group,②6-week calciifcation group,③12-week calciifcation group and④6-week calciifcation + 6-week VK2 group;n=6 in each group. The arterial calciifcation 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: Calciifcation nodule formed in both 6-week and 12-week calciifcation groups, the calciifcation deposition and ROS were higher than Control group,P<0.01. Compared with both calcification groups, the above indexes were decreased in 6-week calciifcation + 6-week VK2 group,P<0.01. Both calciifcation 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 calciifcation is related to oxidative stress injury which may cause the ultra-micro structural damage in smooth muscle cells; VK2 may reduce the oxidative stress injury and improve the condition of vessel calciifcation in experimental rats.