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(胡兹等人)奥皮兹通过减弱肿瘤坏死因子-α诱导的单核细胞与人类脐静脉内皮细胞的黏附来预防动脉粥样硬化形成。

(Huds.) Opiz Prevents Atherogenesis by Attenuating Tumor Necrosis Factor-α-Induced Monocyte Adhesion to Human Umbilical Vein Endothelial Cells.

作者信息

Hamid Adila A, Aminuddin Amilia, Anuar Nur Najmi Mohamad, Mansor Nur Izzati, Ahmad Mohd Faizal, Saleh Mohammed S M, Mokhtar Mohd Helmy, Ugusman Azizah

机构信息

Department of Physiology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur 56000, Malaysia.

Programme of Biomedical Science, Centre for Toxicology and Health Risk Studies, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Kuala Lumpur 50300, Malaysia.

出版信息

Life (Basel). 2022 Sep 20;12(10):1462. doi: 10.3390/life12101462.

Abstract

(Huds.) Opiz is an herb with anti-inflammatory, antioxidant, and anti-atherosclerosis effects. Nevertheless, the mechanism underlying its anti-atherosclerosis effect is poorly comprehended. This study assessed the protective effects of standardized aqueous extract of leaves (PM) on tumor necrosis factor-α (TNF-α)-induced monocyte adhesion to human umbilical vein endothelial cells (HUVEC), which is one of the pivotal early steps in atherogenesis. The results showed that PM decreased the mRNA and protein expression of cellular adhesion molecules, vascular adhesion molecule-1 and intercellular adhesion molecule-1, resulting in reduced adhesion of monocytes to HUVEC. Additionally, PM inhibited nuclear factor kappaB (NF-κB) activation as indicated by reduced NF-κB p65 levels in TNF-α-induced HUVEC. Overall, PM could prevent atherogenesis by inhibiting NF-κB activation and adhesion of monocytes to HUVEC. The effects of PM are probably mediated by its bioactive compound, quercetin-3--glucuronide. The findings may provide a rationale for the anti-atherosclerosis effect of PM, and support its potential use in atherosclerosis.

摘要

奥皮兹是一种具有抗炎、抗氧化和抗动脉粥样硬化作用的草药。然而,其抗动脉粥样硬化作用的潜在机制尚不清楚。本研究评估了叶的标准化水提取物(PM)对肿瘤坏死因子-α(TNF-α)诱导的单核细胞与人脐静脉内皮细胞(HUVEC)黏附的保护作用,这是动脉粥样硬化发生的关键早期步骤之一。结果表明,PM降低了细胞黏附分子、血管细胞黏附分子-1和细胞间黏附分子-1的mRNA和蛋白表达,导致单核细胞与HUVEC的黏附减少。此外,PM抑制了核因子κB(NF-κB)的激活,这表现为TNF-α诱导的HUVEC中NF-κB p65水平降低。总体而言,PM可通过抑制NF-κB激活和单核细胞与HUVEC的黏附来预防动脉粥样硬化的发生。PM的作用可能是由其生物活性化合物槲皮素-3-O-葡萄糖醛酸介导的。这些发现可能为PM的抗动脉粥样硬化作用提供理论依据,并支持其在动脉粥样硬化治疗中的潜在应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e9d/9605558/b14de3717798/life-12-01462-g001.jpg

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