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氧化白藜芦醇通过使脑内皮细胞中的丝裂原活化蛋白激酶（MAPK）和核因子κB（NF-κB）信号失活来减轻脂多糖诱导的炎症和氧化应激。

Oxyresveratrol reduces lipopolysaccharide-induced inflammation and oxidative stress through inactivation of MAPK and NF-κB signaling in brain endothelial cells.

作者信息

Zhou Yan, Deng Qiaowen, Vong Chi Teng, Khan Haroon, Cheang Wai San

机构信息

State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau SAR, China.

Macau Centre for Research and Development in Chinese Medicine, University of Macau, Macau SAR, China.

出版信息

Biochem Biophys Rep. 2024 Sep 7;40:101823. doi: 10.1016/j.bbrep.2024.101823. eCollection 2024 Dec.

DOI:10.1016/j.bbrep.2024.101823
PMID:39290344
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11407036/
Abstract

Inflammatory responses and oxidative stress damage the integrity of the blood-brain barrier (BBB), which is a primary pathological modulator of neurodegenerative diseases. Brain endothelial cells are crucial components of BBB. In the present study, the effect of oxyresveratrol on lipopolysaccharide (LPS)-induced brain endothelial (bEnd.3) cells was assessed. Our results showed that oxyresveratrol diminished protein expressions of inducible nitric oxide synthase (iNOS) and adhesion molecules including intercellular adhesion molecule (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), nitric oxide (NO) production, and proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor (TNF-α) in LPS-elicited bEnd.3 cells. These anti-inflammatory effects were mediated through suppressing nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. In addition, we found that oxyresveratrol reduced reactive oxygen species (ROS) levels. To conclude, the current results demonstrated the protective role of oxyresveratrol against LPS-induced inflammation and oxidative stress in bEnd.3 cells, suggesting its potential effect for mitigating neurodegenerative and cerebrovascular diseases.

摘要

炎症反应和氧化应激会损害血脑屏障（BBB）的完整性，而血脑屏障是神经退行性疾病的主要病理调节因子。脑内皮细胞是血脑屏障的关键组成部分。在本研究中，评估了氧化白藜芦醇对脂多糖（LPS）诱导的脑内皮（bEnd.3）细胞的影响。我们的结果表明，氧化白藜芦醇可降低LPS刺激的bEnd.3细胞中诱导型一氧化氮合酶（iNOS）和包括细胞间黏附分子（ICAM-1）和血管细胞黏附分子-1（VCAM-1）在内的黏附分子的蛋白表达、一氧化氮（NO）的产生以及促炎细胞因子如白细胞介素-6（IL-6）和肿瘤坏死因子（TNF-α）。这些抗炎作用是通过抑制核因子-κB（NF-κB）和丝裂原活化蛋白激酶（MAPK）信号通路介导的。此外，我们发现氧化白藜芦醇降低了活性氧（ROS）水平。总之，目前的结果证明了氧化白藜芦醇对LPS诱导的bEnd.3细胞炎症和氧化应激具有保护作用，表明其对减轻神经退行性疾病和脑血管疾病具有潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/5775b03c67c4/gr7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/1a6cfa351e27/gr3.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/90a1ca553462/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/6138c8127b81/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/5775b03c67c4/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/a61015c23451/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/1fc4fc221696/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/5384db0623a6/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/1a6cfa351e27/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/b0711f7951dc/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/90a1ca553462/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/6138c8127b81/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/237b/11407036/5775b03c67c4/gr7.jpg

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