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孙少卫,杨春芬,童文娟.烟酸姜黄素酯促进血管平滑肌细胞向收缩型转化[J].中国动脉硬化杂志,2019,(3):197~203
烟酸姜黄素酯促进血管平滑肌细胞向收缩型转化
Curcumin trinicotinate promotes vascular smooth muscle cells transformation to contractile type
投稿时间:2018-09-03  修订日期:2018-10-15
DOI:
中文关键词:  烟酸姜黄素酯  血管平滑肌细胞  细胞表型  血管收缩力
英文关键词:curcumin trinicotinate  vascular smooth muscle cell  cell phenotype  vascular contractility
基金项目:湖南省自然科学基金(2016JJ3109);湖南省分子靶标新药研究协同创新中心项目(000200048);湖南省卫生计生委科研计划课题(B20180049)
作者单位E-mail
孙少卫 南华大学药学院 湖南省分子靶标新药研究协同创新中心,湖南省衡阳市 421001 e-mail为sunshaowei2004@aliyun.com,e-mail为313966394@qq.com 
杨春芬 南华大学附属第一医院妇产科,湖南省衡阳市 421001  
童文娟 南华大学附属第一医院妇产科,湖南省衡阳市 421001 e-mail为sunshaowei2004@aliyun.com,e-mail为313966394@qq.com 
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中文摘要:
      目的 研究烟酸姜黄素酯(CurTn)调节血管收缩性的机制及其对血管平滑肌细胞(VSMC)表型调节的影响。方法 将C57BL/6小鼠用50 mg/(kg·d) CurTn灌胃,连续给药6周后取小鼠胸主动脉,用Myography肌动描记仪记录血管收缩力,并检测血管组织中收缩蛋白的水平。将VSMC用10 μmol/L CurTn孵育24 h,Western blot检测VSMC表型相关因子的表达;噻唑蓝法和划痕试验分别观察VSMC的增殖、迁移情况;油红O染色和高效液相色谱分析VSMC对低密度脂蛋白(LDL)的吞噬能力。结果 CurTn灌胃处理的小鼠胸主动脉血管的收缩力增强,且血管平滑肌组织中收缩蛋白的表达增加。CurTn增加VSMC中Myocardin及收缩型特异标志蛋白α-actin和SM22α的表达,同时下调增殖型特异标志物骨桥蛋白的水平。此外,CurTn阻止了VSMC的增殖、迁移及对LDL的吞噬作用。结论 CurTn能增强血管收缩力,其机制可能是通过促进VSMC的收缩表型而阻止其增殖表型来实现的。
英文摘要:
      Aim To explore the mechanism of curcumin trinicotinate (CurTn) regulating vascular contractility and its effect on phenotype regulation of vascular smooth muscle cell (VSMC). Methods C57BL/6 mice were intragastrically administered with 50 mg/(kg·d) CurTn for 6 weeks. The thoracic aorta of the mice was taken after 6 weeks of continuous administration. The contractility of thoracic aorta was examined by tissue myograph system, and the levels of contractile proteins were detected in vascular tissues. VSMCs were treated with 10 μmol/L CurTn for 24 h; Western blot was used to detect the expressions of phenotypic related factors; The proliferation and migration of VSMC were observed by methyl thiazolyl tetrazolium staining and scratch assay; Oil red O staining and high performance liquid chromatography were used to analyze the phagocytosis of low density lipoprotein (LDL) by VSMC. Results The contractility of thoracic aorta vessel was enhanced and the expression of contractile protein in vascular smooth muscle tissue was increased in curTn-treated mice. Our results also showed that CurTn increased the expressions of myocardin and contractile-specific marker proteins α-actin and SM22α in VSMC, and decreased the level of osteopontin, a proliferative-specific marker. Further study found that the migration and proliferation of VSMC were inhibited by CurTn. LDL-treated VSMC was used to detect the effects of CurTn on lipid uptake, and it found that CurTn inhibited the phagocytosis of VSMC. Conclusion CurTn enhances vascular contractility, probably by promoting the contractile phenotype of VSMC and preventing its proliferative phenotype.
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