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大鼠钙化血管尾加压素Ⅱ及其受体上调 被引量:14

Elevated Expression of Urotensin Ⅱ and Its Receptor in Vascular Calcification of Rats
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摘要 目的观察血管钙化大鼠主动脉和心肌尾加压素Ⅱ及其受体表达的变化。方法采用维生素D3和尼古丁诱导大鼠血管钙化模型,以Von Konsa染色检测血管钙化,以原子吸收法和磷酸苯二钠法测定血管钙含量和碱性磷酸酶活性,放射免疫法检测血浆、主动脉和心肌尾加压素Ⅱ含量,免疫组织化学法检测血管尾加压素Ⅱ的表达,RT-PCR法检测主动脉和心肌尾加压素受体mRNA水平。结果维生素D3和尼古丁能够诱导大鼠典型血管钙化形成。Von Kossa染色可见血管钙化大鼠主动脉有大量黑色颗粒沉淀,血管钙含量、碱性磷酸酶活性明显升高,主动脉尾加压素Ⅱ含量、主动脉和心肌尾加压素受体基因表达明显上调。精氨酸饮食能减轻血管钙化,血管钙含量、尾加压素Ⅱ水平及尾加压素受体mRNA表达与单纯钙化组相比轻度下降,但无统计学意义。蛋氨酸饮食能加重血管钙化,增加钙含量,上调尾加压素Ⅱ表达,降低碱性磷酸酶活性。各组之间血浆尾加压素Ⅱ水平差异无统计学意义。结论大鼠钙化血管尾加压素Ⅱ表达上调,提示尾加压素Ⅱ可能参与了血管钙化的发展过程。 Aim To investigate the expression of urotensin Ⅱ(UⅡ) and its receptor(UT) in the aorta and myocardium in a rat model of vascular calcification,and explore the significance of UⅡ system in vascular calcification. Methods Arterial calcification of Sprague-Dawley rats was induced by Vitamin D3 plus nicotine(VDN).Calcification was confirmed by Von Kossa staining and measurement of calcium content.Alkaline phosphatases(ALP) activity was also evaluated.UⅡ contents of plasma,aorta and myocardium were determined by radioimmunoassay,UⅡ immunoactivity and UT mRNA expression were determined by immunohistochemistry and RT-PCR,respectively. Results There were mass black granules deposited in aortic wall of the vascular calcified rats induced by VDN,with Von Kossa staining.Calcium content and ALP activity in calcified aorta of these rats were increased significantly than the control rats(P0.01).Meanwhile,aortic UⅡ and UT mRNA levels in calcified rats,as well as myocardial UT mRNA level,were upregulated significantly compared with the control group.In addition,high arginine diet could reduce the degree of vascular calcification by Von Kossa staining.Calcium contents,UⅡ contents,and UT mRNA levels were slightly lower,but not significantly in the VDN plus arginine rats than in the VDN treated rats.Furthermore,VDN plus high methionine diet treatment could exacerbate vascular calcification.Aortic calcium contents,as well as aortic and myocardial UⅡ contents and UT mRNA expression,were further increased,while aortic ALP activity was decreased in the VDN plus methionine rats than in the calcified rats induced by VDN.There were no significant differences in plasma UⅡ contents among these groups. Conclusion This study found that UⅡ/UT system was significantly increased in calcified vessels,suggesting that UⅡ may be involved in the development of vascular calcification,in a paracrine and/or autocrine manner.
出处 《中国动脉硬化杂志》 CAS CSCD 北大核心 2010年第7期505-509,共5页 Chinese Journal of Arteriosclerosis
基金 国家自然科学基金(30470730和30971273) 广东省自然科学基金(9151051501000016)资助
关键词 尾加压素Ⅱ 尾加压素Ⅱ受体 血管钙化 大鼠 Urotensin Ⅱ Urotensin Ⅱ Receptor Vascular Calcification Rats
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参考文献24

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