法舒地尔联合罗格列酮对脂多糖诱导人冠状动脉内皮细胞MCP-1和VCAM-1表达的影响被引量：2

Effects of fasudil combined with rosiglitazone on expression of MCP-1 and VCAM-1 in lipopolysaccharide-induced human coronary arterial endothelial cells

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摘要目的观察法舒地尔联合罗格列酮对脂多糖（LPS）诱导的人冠状动脉（冠脉）内皮细胞（HCAEC）血管细胞黏附因子1（VCAM-1）、单核细胞趋化因子1（MCP-1）表达的影响。方法选用体外培养的第3~5代HECAC进行实验,将细胞分为空白对照组、LPS组（100 ng/m L LPS作用细胞）、法舒地尔组（10 nmol/L法舒地尔作用细胞）、罗格列酮组（10μg/m L罗格列酮作用细胞）、LPS＋法舒地尔组（先予10 nmol/L的法舒地尔干预细胞2 h后再给予100 ng/m L LPS共同干预22 h）、LPS＋法舒地尔＋罗格列酮组（先予10 nmol/L的法舒地尔和10μg/m L罗格列酮干预细胞2 h后再给予浓度为100 ng/m L LPS共同干预22 h）,实时荧光定量PCR检测各组细胞VCAM-1、MCP-1mRNA,ELISA法检测细胞上清液中可溶性VCAM-1、MCP-1蛋白。结果与空白对照组相比,LPS组细胞VCAM-1、MCP-1 mRNA及上清液VCAM-1、MCP-1蛋白表达高（P均〈0.05）。与LPS组相比,LPS＋法舒地尔组细胞VCAM-1、MCP-1 mRNA及上清液VCAM-1、MCP-1蛋白表达低（P均〈0.05）。与LPS＋法舒地尔组相比,LPS＋法舒地尔＋罗格列酮组细胞VCAM-1、MCP-1 mRNA及上清液VCAM-1、MCP-1蛋白表达低（P均〈0.05）。结论法舒地尔联合罗格列酮可协同抑制LPS诱导的HCAEC中VCAM-1、MCP-1的表达,可能与两者共同抑制p38MAPK、NF-κB信号通路有关。 Objective To observe the effects of fasudil combined with rosiglitazone on the expression of vascular cell adhesion molecule-1 （VCAM-1） and monocyte chemotactic protein 1 （ MCP-1 ） in lipopolysaccharide （LPS） -induced human coronary arterial endothelial cells （HCAECs）. Methods We conducted the experiment using the 3rd to the 5th generation of HCAECs in vitro. Then, the cells were divided into the control group （non-intervention）, LPS group （HCAECs were intervened with 100 ng/mL LPS）, fasudil group （HCAECs were intervened with 10 nmol/L fasudil）, rosiglitazone group （HCAECs were intervened with 10μg/mL rosiglitazone）, LPS ＋ fasudil group （HCAECs were intervened with 10 nmol/L fasudil for 2 h followed by 100 ng/mL LPS for 22 h）, LPS ＋ fasudil ＋ rosiglitazone group （HCAECs were inter-vened with 10 nmol/L fasudil and 10μg/mL rosigtitazone for 2 h followed with 100 ng/mL LPS together for 22 h）. The protein expression of VCAM-1 and MCP-1 in supernatant was detected by ELISA and the mRNA was detected by real-time fluorescent quantification PCR. Results Compared with the control group, the mRNA expression of VCAM-1 and MCP-1, and the protein expression of VCAM-1 and MCP-1 was increased in the LPS group （ all P 〈 0. 05）. Compared with the LPS group, the mRNA expression of VCAM-1 and MCP-1, and the protein expression of VCAM-1 and MCP-1 was decreased in the LPS ＋ fasudil group （all P 〈0.05）. Compared with LPS ＋ fasndil group, the mRNA expression of VCAM-1 and MCP- 1, and the protein expression of VCAM-1 and MCP-1 was decreased in the LPS ＋ fasudil ＋ rosiglitazone group （ all P 〈 0.05 ）. Conclusion Fasudil combined with rosiglitazone collaboratively inhibits the expression of VCAM-1 and MCP-1 in HCAECs induced by LPS, which may be related to their co-suppression of p38MAPK and NF-κB signaling pathway.

作者李世云巫相宏黄文王淳马国添闭奇

机构地区广西医科大学附属第一医院

出处《山东医药》 CAS 北大核心 2016年第23期13-15,共3页 Shandong Medical Journal

基金国家自然科学基金资助项目(81360057)

关键词动脉粥样硬化人冠状动脉内皮细胞血管细胞黏附因子1 单核细胞趋化因子1 atherosclerosis human coronary artery endothelial cells vascular cell adhesion molecule 1 monoeyte ehemotactic protein 1

分类号 R543 [医药卫生—心血管疾病]

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