摘要
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 detect the protective role of L-Arginine in rat vascular calcification and its possible mechanism.Methods Rat vascular calcification model was established by administration of Vitamin D3 and nicotine.SD rats were randomly divided into 6 groups,the control group(CON),the calcification group of vascular calcific model by vitamin D3 and nicotine(VDN),the L-nitro-arginine group(L-NA),the VDN+L-NA(VLN) group,the VDN+ lower L-arginine(VLA) group and the VDN+ higher L-arginine(VHA) group.After Von Kossa staining,vascular calcium content were detected atomic absorption spectrophotometry,and alkaline phosphate activity(APA) and nitric oxide(NO) content were detected by colorimetry,and core binding factor-1(cbfα1) was detected by western blot.Results In VDN group,calcification were observed by Von Kossa staining and significantly higher calcium content and APA were found compared with CON group.Compared with VDN group,significantly lower calcium content and APA were found in VLA and VHA groups.Significantly lower plasma and vascular NO content were found in VDN group compared with CON one.significantly hgher NO content were detected in VLA and VHA groups compared with VDN one.Significantly more expression of cbfα1 protein was found in VDN group compared with CON group and VDN group;significantly less cbfα1 expression were detected in VLA and VHA groups.Conclusion The anti-calcification role of L-arginine might be associated with down regulation of cbfα1 expression.
出处
《宁夏医科大学学报》
2011年第7期619-621,628,F0003,共5页
Journal of Ningxia Medical University
基金
宁夏教育厅资助(宁教高[2005]153号)