Therapeutic effects of chlorogenic acid on allergic rhinitis through TLR4/MAPK/NF-κB pathway modulation

Chlorogenic acid (CGA) exhibits promising anti-inflammatory properties, making it a potential therapeutic agent for inflammatory conditions and allergic rhinitis (AR). This study aimed to evaluate the therapeutic effects of CGA on inflammation in RAW264.7 macrophage cells and on AR in mice. RAW264....

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Main Authors: Xiaoyan Xu, Lei Wang, Guangyao Wu, Xixia Li
Format: Article
Language:English
Published: Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina 2024-12-01
Series:Biomolecules & Biomedicine
Subjects:
Online Access:https://www.bjbms.org/ojs/index.php/bjbms/article/view/11582
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author Xiaoyan Xu
Lei Wang
Guangyao Wu
Xixia Li
author_facet Xiaoyan Xu
Lei Wang
Guangyao Wu
Xixia Li
author_sort Xiaoyan Xu
collection DOAJ
description Chlorogenic acid (CGA) exhibits promising anti-inflammatory properties, making it a potential therapeutic agent for inflammatory conditions and allergic rhinitis (AR). This study aimed to evaluate the therapeutic effects of CGA on inflammation in RAW264.7 macrophage cells and on AR in mice. RAW264.7 cells were treated with lipopolysaccharide (LPS) to induce inflammation and cultured with varying concentrations of CGA, a Tlr4-silenced gene (shTlr4) transfection, and the MAPK/NF-κB pathway activator diprovocim. Cell viability was assessed using the CCK8 assay, while levels of nitric oxide (NO), TNF-α, and IL-6 were measured by Griess colorimetry, immunofluorescence, and ELISA. Expression and phosphorylation levels of the MAPK/NF-κB pathway were evaluated using qPCR and western blotting. Additionally, ovalbumin (OVA)-induced AR mice received different doses of CGA, and Toll-like receptor-4 (Tlr4) overexpression was induced. In vitro, CGA treatment significantly reduced LPS-induced cell activity, NO, TNF-α, and IL-6 secretion, and downregulated Tlr4, p-p38, p-p65, and p-IκB expression. Tlr4 inhibition suppressed cell activity and inflammation by blocking MAPK/NF-κB pathway activation. Conversely, Tlr4 overexpression counteracted the effects of CGA, increasing cell activity and inflammatory factor concentration. In OVA-induced AR mice, CGA effectively alleviated allergic symptoms, reduced inflammatory factor secretion, and inhibited TLR4/MAPK/NF-κB pathway activity. These findings suggest CGA’s potential as an anti-inflammatory agent in RAW264.7 cells and AR models through modulation of the TLR4/MAPK/NF-κB pathway.
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institution Kabale University
issn 2831-0896
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spelling doaj-art-3576bd406fef45f28d2db7f258d060402025-01-06T16:39:05ZengAssociation of Basic Medical Sciences of Federation of Bosnia and HerzegovinaBiomolecules & Biomedicine2831-08962831-090X2024-12-0110.17305/bb.2024.11582Therapeutic effects of chlorogenic acid on allergic rhinitis through TLR4/MAPK/NF-κB pathway modulationXiaoyan Xu0Lei Wang1Guangyao Wu2Xixia Li3Otolaryngology Head and Neck Surgery, China Resources & Wisco General Hospital, Wuhan, Hubei, ChinaOtolaryngology Head and Neck Surgery, China Resources & Wisco General Hospital, Wuhan, Hubei, ChinaOtolaryngology Head and Neck Surgery, China Resources & Wisco General Hospital, Wuhan, Hubei, ChinaOtolaryngology Head and Neck Surgery, China Resources & Wisco General Hospital, Wuhan, Hubei, China Chlorogenic acid (CGA) exhibits promising anti-inflammatory properties, making it a potential therapeutic agent for inflammatory conditions and allergic rhinitis (AR). This study aimed to evaluate the therapeutic effects of CGA on inflammation in RAW264.7 macrophage cells and on AR in mice. RAW264.7 cells were treated with lipopolysaccharide (LPS) to induce inflammation and cultured with varying concentrations of CGA, a Tlr4-silenced gene (shTlr4) transfection, and the MAPK/NF-κB pathway activator diprovocim. Cell viability was assessed using the CCK8 assay, while levels of nitric oxide (NO), TNF-α, and IL-6 were measured by Griess colorimetry, immunofluorescence, and ELISA. Expression and phosphorylation levels of the MAPK/NF-κB pathway were evaluated using qPCR and western blotting. Additionally, ovalbumin (OVA)-induced AR mice received different doses of CGA, and Toll-like receptor-4 (Tlr4) overexpression was induced. In vitro, CGA treatment significantly reduced LPS-induced cell activity, NO, TNF-α, and IL-6 secretion, and downregulated Tlr4, p-p38, p-p65, and p-IκB expression. Tlr4 inhibition suppressed cell activity and inflammation by blocking MAPK/NF-κB pathway activation. Conversely, Tlr4 overexpression counteracted the effects of CGA, increasing cell activity and inflammatory factor concentration. In OVA-induced AR mice, CGA effectively alleviated allergic symptoms, reduced inflammatory factor secretion, and inhibited TLR4/MAPK/NF-κB pathway activity. These findings suggest CGA’s potential as an anti-inflammatory agent in RAW264.7 cells and AR models through modulation of the TLR4/MAPK/NF-κB pathway. https://www.bjbms.org/ojs/index.php/bjbms/article/view/11582Chlorogenic acidCGARAW264.7 cellsallergic rhinitisARTLR4/MAPK/NF-κB pathway
spellingShingle Xiaoyan Xu
Lei Wang
Guangyao Wu
Xixia Li
Therapeutic effects of chlorogenic acid on allergic rhinitis through TLR4/MAPK/NF-κB pathway modulation
Biomolecules & Biomedicine
Chlorogenic acid
CGA
RAW264.7 cells
allergic rhinitis
AR
TLR4/MAPK/NF-κB pathway
title Therapeutic effects of chlorogenic acid on allergic rhinitis through TLR4/MAPK/NF-κB pathway modulation
title_full Therapeutic effects of chlorogenic acid on allergic rhinitis through TLR4/MAPK/NF-κB pathway modulation
title_fullStr Therapeutic effects of chlorogenic acid on allergic rhinitis through TLR4/MAPK/NF-κB pathway modulation
title_full_unstemmed Therapeutic effects of chlorogenic acid on allergic rhinitis through TLR4/MAPK/NF-κB pathway modulation
title_short Therapeutic effects of chlorogenic acid on allergic rhinitis through TLR4/MAPK/NF-κB pathway modulation
title_sort therapeutic effects of chlorogenic acid on allergic rhinitis through tlr4 mapk nf κb pathway modulation
topic Chlorogenic acid
CGA
RAW264.7 cells
allergic rhinitis
AR
TLR4/MAPK/NF-κB pathway
url https://www.bjbms.org/ojs/index.php/bjbms/article/view/11582
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