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目的探讨L-精氨酸(L-arginine,L-Arg)对大鼠血管钙化的作用及其机制。方法利用维生素D3、尼古丁制备大鼠血管钙化模型,并将大鼠随机分为6组:对照组(CON)、钙化组(VDN)、L-NAME组(L-NA)、钙化+L-NAME组(VLN)、钙化+低剂量L-Arg组(VLA)、钙化+高剂量L-Arg组(VHA)。常规饲养6周后采集标本,胸主动脉行Von Kossa染色,用原子吸收分光光度法检测大鼠血管组织钙含量、碱性磷酸酶活性及NO含量,western blot技术检测核心结合因子1(core binding factor-1,cbfα1)的表达。结果 VonKossa染色,VDN组明显见到钙化颗粒,并成片状,使用L-Arg干预后钙化颗粒明显减少;VDN组的血管组织钙含量、碱性磷酸酶活性较CON组均明显增加(P<0.05),VLA与VHA组血管组织钙含量、碱性磷酸酶活性均较VDN组明显降低(P<0.05);VDN组血管组织NO含量较CON组明显减少(P<0.05),VLA与VHA组均较VDN组升高(P<0.05);western blot检测表明,VDN组cbfα1表达水平较CON组明显升高(P<0.05),VLA与VHA组较VDN组明显降低(P<0.05)。结论 L-Arg可能通过降低核心结合因子1的表达起到减轻血管钙化的作用。
Objective To investigate the effect of L-arginine (L-Arginine) on vascular calcification in rats and its mechanism. Methods Vascular calcification model was made by vitamin D3 and nicotine. The rats were randomly divided into 6 groups: CON, VDN, L-NAME, L-NAME (VLN), calcification + low dose L-Arg group (VLA) and calcific + high dose L-Arg group (VHA). The samples were collected 6 weeks after routine feeding. Von Kossa staining was performed on the thoracic aorta. The contents of calcium, alkaline phosphatase and NO were detected by atomic absorption spectrophotometry. The expressions of core binding factor 1 factor-1, cbfα1). Results Von Kossa staining showed that calcified granules were found in VDN group, and the calcification granules were obviously reduced after intervention with L-Arg. Calcium content and alkaline phosphatase activity of vascular tissue in VDN group were significantly increased compared with CON group (P < 0.05). The contents of calcium and alkaline phosphatase in vascular tissue of VLA and VHA groups were significantly lower than those of VDN group (P <0.05). The content of NO in VDN group was significantly lower than that of CON group (P <0.05) (P <0.05). Compared with VDN group, the expression of cbfα1 in VDN group was significantly higher than that in CON group (P <0.05), while VLA and VHA groups were significantly lower than those in VDN group (P <0.05). Conclusion L-Arg may play a role in reducing vascular calcification by decreasing the expression of core-binding factor-1.