Astragaloside IV suppresses inflammatory response via suppression of NF-κB, and MAPK signalling in human bronchial epithelial cells. (4th May 2022)

• Record Type: Journal Article
• Authors: Hsieh, Hsi-Lung; Liu, Shih-Hai; Chen, Ya-Ling; Huang, Chien-Yi; Wu, Shu-Ju
• Is Part Of: Archives of physiology and biochemistry. Volume 128:Number 3(2022)
• Page Start: 757
• Page End: 766
• Publication Date: 2022-05-04
• Subjects: Astragaloside IV -- bronchial epithelial cells -- inflammation -- MAPK -- NF-κB; Physiology -- Periodicals; Biochemistry -- Periodicals; Biophysics -- Periodicals; Biochemistry; Physiology; 571
• DOI: 10.1080/13813455.2020.1727525
• Languages: English
• ISSNs: 1381-3455

Abstract

Abstract: Context: Astragaloside IV isolated from Astragalus membranaceus (Fisch.), which was reported to have anti-tumor, anti-asthma, and suppressed cigarette smoke-induced lung inflammation in mice. Objectives: This study investigated whether astragaloside IV reduced the expression of inflammatory mediators and oxidative stress in BEAS-2B cells. Methods: BEAS-2B cells treated with astragaloside IV, and then stimulated with TNF-α or TNF-α/IL-4. The levels of cytokine and chemokine were analysed with ELISA and real-time PCR. Results: Astragaloside IV significantly inhibited the levels of CCL5, MCP-1, IL-6 and IL-8. Astragaloside IV also reduced ICAM-1 expression for blocked THP-1 monocyte adhesion to BEAS-2B cells. Furthermore, astragaloside IV attenuated the phosphorylation of MAPK, and reduced the translocation of p65 into the nucleus. Astragaloside IV could increase the expression of HO-1 and Nrf2 for promoting the oxidant protective effect. Conclusion: Aastragaloside IV has an anti-inflammatory and oxidative effect via regulated NF-κB, MAPK and HO-1/Nrf2 signalling pathways in human bronchial epithelial cells.