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Isorhamnetin attenuates TNF-α-induced inflammation, proliferation, and migration in human bronchial epithelial cells via MAPK and NF-κB pathways.

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机构: [1]The First Clinical School, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China [2]Department of Anaesthesiology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China [3]Department of Encephalology, Yangjiang People's Hospital, Yangjiang, Guangdong, China
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关键词: asthma inflammation isorhamnetin MAPK nuclear factor-κB

摘要:
Isorhamnetin has distinct anti-inflammatory activity and inhibits cell proliferation and migration. These effects are also involved in the pathogenesis of asthma. However, the effect of isorhamnetin on bronchial epithelial cells in patients with asthma has not been examined. Cells of human bronchial epithelial cell line BEAS-2B were cultured with isorhamnetin and tumour necrosis factor (TNF)-α. The effects of isorhamnetin on BEAS-2B cell viability were assessed using CCK8 assay. The EdU (5-ethynyl-2'-deoxyuridine) cell proliferation assay was performed to assess cell proliferation. BEAS-2B cell migration was measured using Transwell and wound healing assays. Real-time PCR and enzyme-linked immunosorbent assay were conducted to measure the expression of pro-inflammatory cytokines. Protein expression levels were determined by western blotting. Immunofluorescence was used to detect nuclear translocation of nuclear factor kappa B (NF-κB). We found that isorhamnetin at 20 and 40 μM reduced the proliferation of BEAS-2B cells induced by TNF-α. Isorhamnetin significantly decreased the expression of interleukin (IL)-1β, IL-6, IL-8, and C-X-C motif chemokine ligand 10 in BEAS-2B cells induced by TNF-α. Additionally, 10 μM isorhamnetin effectively reduced cell migration induced by TNF-α. Treatment with isorhamnetin inhibited the phosphorylation of mitogen-activated protein kinase (MAPK) and NF-κB pathways induced by TNF-α. In summary, isorhamnetin inhibited the inflammation, proliferation, and migration of BEAS-2B cells by regulating the MAPK and NF-κB signalling pathways and is a drug candidate for asthma. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.

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出版当年[2020]版:
大类 | 4 区 医学
小类 | 4 区 解剖学与形态学
最新[2025]版:
大类 | 4 区 医学
小类 | 3 区 解剖学与形态学
第一作者:
第一作者机构: [1]The First Clinical School, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China [2]Department of Anaesthesiology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China
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通讯机构: [1]The First Clinical School, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China [2]Department of Anaesthesiology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China [*1]Department of Anaesthesiology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, 16 Jichang Road, Guangzhou, Guangdong 510405, China
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