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减弱肿瘤坏死因子-α诱导的人脐静脉内皮细胞中血管细胞黏附分子-1和细胞间黏附分子-1的表达。

attenuates TNF-α-induced VCAM-1 and ICAM-1 expression in human umbilical vein endothelial cells.

作者信息

Ismail Siti M, Sundar Uma M, Hui Chua K, Aminuddin Amilia, Ugusman Azizah

机构信息

Department of Physiology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latiff, Cheras, Kuala Lumpur, Malaysia.

出版信息

J Taibah Univ Med Sci. 2018 Feb 21;13(3):225-231. doi: 10.1016/j.jtumed.2018.01.003. eCollection 2018 Jun.

DOI:10.1016/j.jtumed.2018.01.003
PMID:31435328
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6694970/
Abstract

OBJECTIVES

Inflammation plays a key role in the pathogenesis of atherosclerosis. is an herb with antioxidant and anti-atherosclerotic activities. The aim of this study was to evaluate the anti-inflammatory properties of an aqueous extract of (AEPS) in human umbilical vein endothelial cells (HUVECs).

METHODS

HUVECs were divided into six groups: control, treatment with 10 ng/ml TNF-α, and co-treatment of 10 ng/ml TNF-α with four different concentrations of AEPS (100, 150, 250, and 300 μg/ml) for 24 h. Subsequently, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) protein expression, U937 monocyte cells adhesion, and nuclear factor-kappaB (NF-κB) p65 expression in HUVECs were measured.

RESULTS

Treatment of TNF-α-stimulated HUVECs with AEPS at different concentrations resulted in decreased VCAM-1 and ICAM-1 protein expression in a dose-dependent manner. Furthermore, AEPS also inhibited TNF-α-stimulated U937 monocyte cells adhesion to HUVECs. In addition, AEPS reduced TNF-α-induced NF-κB p65 expression in a dose-dependent manner.

CONCLUSIONS

The results indicated that AEPS suppressed TNF-α-induced VCAM-1 and ICAM-1 expression NF-κB signaling.

摘要

目的

炎症在动脉粥样硬化的发病机制中起关键作用。[某种草药名称]是一种具有抗氧化和抗动脉粥样硬化活性的草药。本研究的目的是评估[某种草药名称]水提取物(AEPS)对人脐静脉内皮细胞(HUVECs)的抗炎特性。

方法

将HUVECs分为六组:对照组、用10 ng/ml肿瘤坏死因子-α(TNF-α)处理组,以及用10 ng/ml TNF-α与四种不同浓度(100、150、250和300 μg/ml)的AEPS共同处理24小时的组。随后,检测HUVECs中血管细胞黏附分子-1(VCAM-1)和细胞间黏附分子-1(ICAM-1)蛋白表达、U937单核细胞黏附以及核因子-κB(NF-κB)p65表达。

结果

用不同浓度的AEPS处理TNF-α刺激的HUVECs导致VCAM-1和ICAM-1蛋白表达呈剂量依赖性降低。此外,AEPS还抑制TNF-α刺激的U937单核细胞与HUVECs的黏附。另外,AEPS以剂量依赖性方式降低TNF-α诱导的NF-κB p65表达。

结论

结果表明AEPS抑制TNF-α诱导的VCAM-1和ICAM-1表达及NF-κB信号传导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6589/6694970/16d06de20ea4/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6589/6694970/7458fc0f18aa/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6589/6694970/41633b803a60/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6589/6694970/6664a48b477f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6589/6694970/16d06de20ea4/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6589/6694970/7458fc0f18aa/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6589/6694970/41633b803a60/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6589/6694970/6664a48b477f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6589/6694970/16d06de20ea4/gr4.jpg

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