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机构地区:[1]山东大学医学院,济南250100 [2]济宁医学院附属医院心内二科
出 处:《临床心血管病杂志》2015年第10期1106-1111,共6页Journal of Clinical Cardiology
基 金:山东省自然科学基金项目(No:ZR2011HL006)
摘 要:目的:研究黄芪甲苷(AS-IV)对肿瘤坏死因子(TNF-α)诱导的大鼠胸主动脉平滑肌细胞(A7r5细胞)增殖、迁移的影响。方法:建立体外TNF-α诱导的A7r5细胞增殖、迁移模型,用不同浓度AS-IV进行干预。应用WST-8法检测细胞增殖活性,用划痕实验和Transwell侵袭实验分别检测细胞迁移、侵袭能力。结果:A7r5细胞经TNF-α作用后,其增殖活性、迁移距离、侵袭能力均明显增加,与对照组相比有显著性差异(P<0.05);而经AS-IV干预后,细胞增殖活性降低、迁移距离变短、侵袭能力下降,与TNF-α组相比有显著性差异(P<0.05),并且这种药物抑制作用呈时间与剂量依赖性。结论:AS-IV可抑制TNF-α诱导的血管平滑肌细胞增殖、迁移,这可能是AS-IV预防和治疗血管再狭窄、动脉粥样硬化等血管增生性疾病的作用机制之一。Objective:To investigate the effects of Astragaloside IV(AS-IV)on proliferation and migration of rat vascular smooth muscle cells from thoracic aorta(A7r5cells)that were induced by tumor necrosis factor-α(TNF-α).Method:The model of A7r5 cells proliferation and migration was established by TNF-αinducer in vitro,and intervened by different concentrations of AS-IV.A WST-8assay was used to evaluate cell proliferation activity.Wound migration assay and Transwell invasion assay were used to analyze cell migratory and invasive capability.Result:The proliferative activity,migratory distance and invasive capacity of A7r5 cells were obviously increased in the TNF-αgroup.There was a significant difference as compared with the control group(P〈0.05).But when pretreated with AS-IV ahead of time,the proliferative activity,migratory distance and invasive capacity of A7r5 cells were decreased in a time-and dose-dependent manner.There was a significant difference as compared with the TNF-αgroup(P〈0.05).Conclusion:AS-IV exerts inhibitory effects on vascular smooth muscle cells proliferation and migration,which may be one of the mechanisms that AS-IV can prevent and treat the vascular proliferative diseases such as reangiostenosis and atherosclerosis.
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