Isobavachalcone attenuates Sephadex-induced lung injury via activation of A20 and NRF2/HO-1 in rats

• Published in: European journal of pharmacology 2019-04, Vol.848, p.49-54
• Main Authors: Gao, Dehong, Liu, Feng, Li, Zhipeng, Guan, Yifu
• Format: Article
• Language: English
• Subjects: A20; Acute Lung Injury - chemically induced; Acute Lung Injury - drug therapy; Acute Lung Injury - metabolism; Animals; Chalcones - pharmacology; Chalcones - therapeutic use; Dextrans - toxicity; DNA-Binding Proteins - agonists; DNA-Binding Proteins - metabolism; Dose-Response Relationship, Drug; Heme Oxygenase-1 - metabolism; Isobavachalcone; Lung injury; Male; Membrane Proteins - agonists; Membrane Proteins - metabolism; NF-E2-Related Factor 2 - agonists; NF-E2-Related Factor 2 - metabolism; NF-κB; NRF2/HO-1; Rats; Rats, Sprague-Dawley
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/j.ejphar.2019.01.034

The aim of this study is to investigate the protective effect and underlying molecular mechanisms of isobavachalcone on Sephadex-induced lung injury in rats. The result showed isobavachalcone inhibited massive granulomas, decreased inflammatory cells infiltration and oxidative stress markers level, but it can increase antioxidant enzymes level. The ELISA assay exhibited isobavachalcone decreased TNF-α production in BALF and lung tissue. Western blotting analysis showed isobavachalcone can inhibit NF-κB pathway that may be mediated by upregulation of A20. Furthermore, we also found isobavachalcone can activate NRF2/HO-1 pathway and inhibit adhesion molecule expression. Taken together, the present results suggested that isobavachalcone can attenuate Sephadex-induced lung injury that may be related to inhibition of NF-κB mediated by upregulation of A20 and activation of NRF2/HO-1 signaling pathway.