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作 者:吴德虎 唐慧莉[1] 陈慧[2] WU De-hu;TANG Hui-li;CHEN Hui(Department of Cardiology,People's Hospital of Anji,Anji 313300,China;Department of Preventive Treatment,Traditional Chinese Medical Hospital of Xiaoshan District,Hangzhou 311201,China)
机构地区:[1]浙江省安吉县人民医院心血管内科,安吉313300 [2]杭州市萧山区中医院治未病科,杭州311201
出 处:《浙江中西医结合杂志》2022年第8期710-715,共6页Zhejiang Journal of Integrated Traditional Chinese and Western Medicine
基 金:浙江省医药卫生科技计划项目(No.2021KY965)。
摘 要:目的探讨松香酸对急性心肌梗死(AMI)后内皮细胞血管生成及迁移的作用与机制。方法在体外构建人脐静脉血管内皮细胞(human umbilical vein endothelial cells,HUVECs)细胞缺氧模型;通过Matrigel小管形成实验检测HUVECs的血管生成情况;Transwell及伤口愈合实验检测HUVECs的细胞迁移;Western blot检测血管内皮生成因子A(VEGFA)的表达情况;qRT-PCR检测miR-30a-3p的转录水平。结果成功构建细胞缺氧模型;Matrigel小管形成实验显示缺氧抑制HUVECs的血管生成及细胞迁移,而利用松香酸处理缺氧细胞后,可以促进其血管生成和细胞迁移;Western blot结果显示,松香酸能够促进VEGFA的表达;进一步利用qRT-PCR检测松香酸处理后细胞内miR-30a-3p水平,发现松香酸可明显提高miR-30a-3p水平,而在细胞内转染miR-30a-3p inhibitor后,松香酸促进HUVECs的血管生成和细胞迁移作用被抑制。结论松香酸可能通过调节miR-30a-3p的表达,增强HUVECs的血管生成与细胞迁移。Objective To assess the effect and underlying mechanism of abietic acid on regulation of endothelial cell angiogenesis and migration in an in vitro model of acute myocardial infarction(AMI).Methods The hypoxia model of human umbilical vein endothelial cells(HUVECs)was established in vitro to assess HUVECs angiogenesis using the Matrigel tubule formation assay.Transwell and wound healing assays were performed to detect HUVECs migration,while Western blot was used to detect level of vascular endothelial growth factor A(VEGFA)and qRT-PCR was to detect level of miR-30a-3p.Results This HUVECs hypoxia model was successfully constructed and showed that hypoxia inhibited HUVECs angiogenesis and migration.Treatment of hypoxic cells with abietic acid was able to promote HUVECs angiogenesis and migration.Moreover,abietic acid treatment also induced VEGFA expression and significantly increased miR-30a-3p level.However,transfection of miR-30a-3p inhibitor blocked the effect of abietic acid-induced HUVECs angiogenesis and migration.Conclusion Abietic acid was able to enhance HUVECs angiogenesis and migration by upregulation of miR-30a-3p expression in HUVECs.
关 键 词:AMI 松香酸 miR-30a-3p HUVECS
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