脂联素对小鼠主动脉平滑肌细胞体外钙化作用机制的研究  

Study on Adiponectin for Inhibiting the Calcification in Cultured Aortic Smooth Muscle Cell of Rats via Signaling Pathway

作　　者：刘婷[1] 邵挥戈[1] 黄碧[1] 赵立玲[2] 

机构地区：[1]湖南省长沙市中心医院内分泌科,湖南长沙410004 [2]中南大学湘雅二医院代谢内分泌研究所,湖南长沙410011

出　　处：《医学临床研究》2013年第4期642-644,共3页Journal of Clinical Research

摘　　要：【目的】探讨脂联素对主动脉平滑肌细胞（ASMCs）体外钙化的作用机制。【方法]体外培养脂联素基因敲除小鼠ASMCs，以a-磷酸奈酚法检测钙化指标碱性磷酸酶（AI。P），WesternBlot检测脂联素受体（AdipoR）表达及丝裂原活化蛋白激酶（MAPK）激活。siRNA—AdipoR或加用MAPK信号转导阻断剂，观察脂联素对ASMCs钙化作用的变化。【结果】在小鼠ASMCs检测出AdipoR1表达。脂联素干预后激活p38MAPK。若抑制AdipoRl表达或使用p38MAPK信号转导阻断剂SB203580，脂联素抑制ALP活性的作用消失。【结论】脂联素通过AdipoRl／p38信号转导途径抑制小鼠ASMCs体外钙化。[Objective]To explore the mechanism of the effect of adiponectin on calcification in cultured aortic smooth muscle celIs（ASMCs）. [Methods] In cultured ASMCs of adiponectin-/- mice, alkaline phos- phatase（ALP） activity was measured by using ct-nitrophenyl phosphate as substrate. Adiponectin receptor（Ad- ipoR） and mitogen-activated protein kinase（MAPK） were analyzed by Western Blot. The change of the effect of adiponectin on ASMCs calcification was observed by using AdipoR1 siRNA or additionally using MAPK sig- nal transduction pathway. [Resuhs]AdipoR1 expression was detected in ASMCs rats. After adiponectin inter- ference, p38 MAPK was activated. If AdipoR1 expression was inhibited or p38 MAPK signal transduction in- hibitor SB203580 was used, the effect of adiponectin for inhibiting ALP activity disappeared. [Conclusion] Ad- iponectin inhibits ASMCs calcification of rats in vitro via AdipoR1/p38 signaling pathway.

关 键 词：脂联素 主动脉 肌细胞 平滑肌 钙化 生理性 信号传导 小鼠 

分 类 号：R36[医药卫生—病理学]