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Abstract Title:

Astragaloside IV suppresses inflammatory response via suppression of NF-κB, and MAPK signalling in human bronchial epithelial cells.

Abstract Source:

Arch Physiol Biochem. 2020 Feb 14:1-10. Epub 2020 Feb 14. PMID: 32057253

Abstract Author(s):

Hsi-Lung Hsieh, Shih-Hai Liu, Ya-Ling Chen, Chien-Yi Huang, Shu-Ju Wu

Article Affiliation:

Hsi-Lung Hsieh

Abstract:

Astragaloside IV isolated from(Fisch.), which was reported to have anti-tumor, anti-asthma, and suppressed cigarette smoke-induced lung inflammation in mice.This study investigated whether astragaloside IV reduced the expression of inflammatory mediators and oxidative stress in BEAS-2B cells.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.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.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.

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