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阿魏酸钠对人动脉平滑肌细胞和内皮细胞作用的机制研究
引用本文:朱晓斐,李江,王宝,李玉骞,赵振伟.阿魏酸钠对人动脉平滑肌细胞和内皮细胞作用的机制研究[J].现代生物医学进展,2014,14(16):3046-3050.
作者姓名:朱晓斐  李江  王宝  李玉骞  赵振伟
作者单位:[1]成都军区昆明总医院神经内科,云南昆明650001 [2]第四军医大学唐都医院神经外科,陕西西安710038
基金项目:国家自然科学基金项目(81101022)
摘    要:目的:研究阿魏酸钠(SF)对人主动脉平滑肌(HASMC)和内皮细胞(HAEC)的影响,探讨SF成为抑制支架内再狭窄药物的机制。方法:HASMC和HAEC经SF处理后(0-1000μg/ml),用CCK-8试剂和划痕愈合试验检测不同药物浓度对两种生长和细胞迁移能力的影响;采用免疫细胞化学和Western blot检测HAECs中FoxM1和VEGF的表达。结果:SF对两种细胞的作用呈剂量依赖性,SF在10-1000μg/ml浓度时,HASMC的生长活力明显降低,在0.1-100μg/mlHAECs生长活力显著增强(P0.05)。在1-1000μg/ml浓度下HASMCs迁移能力受到抑制,HAECs的迁移能力明显增加(0.1-100μg/ml)(P0.05)。同时HAECs内FoxM1和VEGF表达明显增高(P0.05),程度与SF浓度有剂量依赖关系。结论:阿魏酸钠能抑制血管平滑肌的增值和迁移;同时增加内皮细胞FoxM1和VEGF的表达,促进内皮细胞的增值和迁移,这些特征使其可能成为抑制支架内再狭窄的药物。

关 键 词:阿魏酸钠  血管细胞  抑制再狭窄

Effects and Mechanisms of SodiumFerulate on Human Aortic Soomth Muscle Cells and Endothelial Cells
ZHU Xiao-fei,LI Jiang,WANG Bao,LI Yu-qian,ZHAO Zhen-wei.Effects and Mechanisms of SodiumFerulate on Human Aortic Soomth Muscle Cells and Endothelial Cells[J].Progress in Modern Biomedicine,2014,14(16):3046-3050.
Authors:ZHU Xiao-fei  LI Jiang  WANG Bao  LI Yu-qian  ZHAO Zhen-wei
Institution:1 Department of Neurology, Kunming General Hospital of PLA, Kunming, Yunnan, 650001, China; 2 Department ofNeurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China)
Abstract:Objective: To study the effects and mechanisms of Sodium ferulate (SF) on human aortic soomth muscle cells (HASMCs) and endothelial cells (HAECs) to approach its potential possibility for in-stent restenosis. Methods: HASMCs and HAECs were treated with different concentrations of SF and divided into 6 groups (0 μg/ml, 0.1 μg/ml, 1 μg/ml,10μg/ml, 100μg/ml, and 1000 μg/ml).Cell viability was determined by CCK-8 kit. Cell migration distance was evaluated by Scratch wound healing assay. Changes of FoxM1 and VEGF expression in HAECs were detected through the Immtmocytochemistry method, Western blot and image analysis. Results: SF inhibited proliferation and migration of HASMCs in a does-dependent manner (10-1000 μg/ml) (P 〈0.05 ). However, SF promoted proliferation and migration of HAECs in a dose-dependent manner (0.1-100 μg/ml) (P 〈 0.05 ). The expression of FoxM 1 and VEGF was increased in a does-dependent manner in HAECs (P 〈0.05). Conclusion:SF may inhibit proliferation of HASMCs, and promote vascular endothelial healing through increasing the expression of FoxM1 and VEGF. It suggests that SF may be an effective agent for in-stent restenosis.
Keywords:HASMCs  HAECs  In-stent restenosis
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