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非洲吊灯树的甲醇提取物通过下调晚期糖基化终末产物受体(RAGE)和黏附分子,在内皮细胞中发挥抗动脉粥样硬化作用。

Methanolic extract of Kigelia africana exhibits antiatherosclerotic effects in endothelial cells by downregulating RAGE and adhesion molecules.

作者信息

Ko Y S, Nash O, Choi S, Kim H J

机构信息

Department of Pharmacology, School of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju, 52727, Korea.

Institute of Advanced Medical Research and Training, College of Medicine, University of Ibadan, Nigeria.

出版信息

Trop Biomed. 2019 Mar 1;36(1):172-182.

Abstract

The Kigelia plant is used in African countries for its medicinal properties. Kigelia africana is an interesting example of a medicinal plant due to its pharmacological activities, including its anti-inflammatory effect. Atherosclerosis, the primary cause of cardiovascular disease, is related to lipoprotein oxidation, inflammation and immune responses involving the vascular endothelium and immune cells. Therefore, in this study we investigated the effects of Kigelia africana (Lam.) extract, focusing particularly on antiatherosclerotic effects in endothelial cells (ECs). The methanolic extract of Kigelia africana (MKA) showed no cytotoxicity on ECs at doses of 10~200 µg/ml. MKA reduced RAGE expression on oxLDL- or TNF-α-stimulated ECs in a dose dependent manner, showing significant inhibition at a concentration of 50 µg/ml. In addition, MKA significantly inhibited the oxLDL- or TNF-αinduced expression of vascular cell adhesion molecule-1 (VCAM-1) in ECs in a dose-dependent manner but did not affect intracellular adhesion molecule-1 (ICAM-1), resulting in downregulation of the migration and adhesion of THP-1 monocytes to ECs. These results suggest that MKA could be used for the treatment of atherosclerosis without cytotoxicity.

摘要

在非洲国家,香肠树因其药用特性而被使用。由于其药理活性,包括抗炎作用,非洲香肠树是一种有趣的药用植物实例。动脉粥样硬化是心血管疾病的主要原因,与脂蛋白氧化、炎症以及涉及血管内皮和免疫细胞的免疫反应有关。因此,在本研究中,我们研究了非洲香肠树提取物的作用,特别关注其对内皮细胞(ECs)的抗动脉粥样硬化作用。非洲香肠树甲醇提取物(MKA)在10~200μg/ml剂量下对ECs无细胞毒性。MKA以剂量依赖性方式降低了氧化型低密度脂蛋白(oxLDL)或肿瘤坏死因子-α(TNF-α)刺激的ECs上的晚期糖基化终末产物受体(RAGE)表达,在浓度为50μg/ml时显示出显著抑制作用。此外,MKA以剂量依赖性方式显著抑制了ECs中oxLDL或TNF-α诱导的血管细胞黏附分子-1(VCAM-1)表达,但不影响细胞间黏附分子-1(ICAM-1),从而导致THP-1单核细胞向ECs的迁移和黏附下调。这些结果表明,MKA可用于治疗动脉粥样硬化且无细胞毒性。

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