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18β-Glycyrrhetinic acid suppresses allergic airway inflammation through NF-κB and Nrf2/HO-1 signaling pathways in asthma mice.

ABSTRACT: 18β-Glycyrrhetinic acid (18β-GA), the main bioactive component of Glycyrrhizae Radix, is considered a promising anti-inflammatory and antioxidant agent. Here, we evaluated the anti-inflammatory and antioxidant effects of 18β-GA in an ovalbumin (OVA)-induced asthma mouse model, and examined the role of NF-κB and Nrf2/HO-1 signaling pathways. The histopathological changes of lung tissue in mouse were assessed by histochemical staining and counting of inflammatory cells. The levels of IgE and inflammatory cytokines in the bronchoalveolar lavage fluid of mice were detected by ELISA. In OVA-induced asthmatic mice, 18β-GA treatment can significantly improve lung function and reduce lung inflammation including infiltration of inflammatory cells. In addition, 18β-GA reduced the OVA-induced NF-κB phosphorylation in lungs of mice while increasing the expression of Nrf2 and HO-1. These results indicate that 18β-GA protects OVA-induced allergic inflammation of airway by inhibiting phosphorylation of NF-κB and enhancing the Nrf2/HO-1 pathway, and serves as a potential treatment option for allergic inflammation of airway.

SUBMITTER: Liu J

PROVIDER: S-EPMC8873505 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature

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18β-Glycyrrhetinic acid suppresses allergic airway inflammation through NF-κB and Nrf2/HO-1 signaling pathways in asthma mice.

Liu Jianming J Xu Yanqi Y Yan Minyu M Yu Yingjie Y Guo Yongmei Y

Scientific reports 20220224 1

18β-Glycyrrhetinic acid (18β-GA), the main bioactive component of Glycyrrhizae Radix, is considered a promising anti-inflammatory and antioxidant agent. Here, we evaluated the anti-inflammatory and antioxidant effects of 18β-GA in an ovalbumin (OVA)-induced asthma mouse model, and examined the role of NF-κB and Nrf2/HO-1 signaling pathways. The histopathological changes of lung tissue in mouse were assessed by histochemical staining and counting of inflammatory cells. The levels of IgE and infla ...[more]

PMID: 35210449

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Project description:BackgroundAngiotensin (Ang)-(1-7) can reduce airway inflammation and airway remodeling in allergic asthma. Autophagy-related 5 (ATG5) has attracted wide attentions in asthma. However, the effects of Ang-(1-7) on ATG5-mediated autophagy in allergic asthma are unclear.MethodsIn this study, human bronchial epithelial cell (BEAS-2B) and human bronchial smooth muscle cell (HBSMC) were treated with different dose of Ang-(1-7) to observe changes of cell viability. Changes of ATG5 protein expression were measured in 10 ng/mL of interleukin (IL)-13-treated cells. Transfection of ATG5 small interference RNA (siRNA) or ATG5 cDNA in cells was used to analyze the effects of ATG5 on secretion of cytokines in the IL-13-treated cells. The effects of Ang-(1-7) were compared to the effects of ATG5 siRNA transfection or ATG5 cDNA transfection in the IL-13-treated cells. In wild-type (WT) mice and ATG5 knockout (ATG5-/-) mice, ovalbumin (OVA)-induced airway inflammation, fibrosis and autophagy were observed. In the OVA-induced WT mice, Ang-(1-7) treatment was performed to observe its effects on airway inflammation, fibrosis and autophagy.ResultsThe results showed that ATG5 protein level was decreased with Ang-(1-7) dose administration in the IL-13-treated BEAS-2B and IL13-treated HBSMC. Ang-(1-7) played similar results to ATG5 siRNA that it suppressed the secretion of IL-25 and IL-13 in the IL-13-treated BEAS-2B cells, and inhibited the expression of transforming growth factor (TGF)-β1 and α-smooth muscle actin (α-SMA) protein in the IL-13-treated HBSMC cells. ATG5 cDNA treatment significantly increased the secretion of IL-25 and IL-13 and expression of TGF-β1 and α-SMA protein in IL-13-treated cells. Ang-(1-7) treatment suppressed the effects of ATG5 cDNA in the IL-13-treated cells. In OVA-induced WT mice, Ang-(1-7) treatment suppressed airway inflammation, remodeling and autophagy. ATG5 knockout also suppressed the airway inflammation, remodeling and autophagy.ConclusionsAng-(1-7) treatment suppressed airway inflammation and remodeling in allergic asthma through inhibiting ATG5, providing an underlying mechanism of Ang-(1-7) for allergic asthma treatment.

Dataset Information

18β-Glycyrrhetinic acid suppresses allergic airway inflammation through NF-κB and Nrf2/HO-1 signaling pathways in asthma mice.

Publications

18β-Glycyrrhetinic acid suppresses allergic airway inflammation through NF-κB and Nrf2/HO-1 signaling pathways in asthma mice.

Similar Datasets

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