Crocin reduces Aspergillus fumigatus‐induced airway inflammation and NF‐κB signal activation. Issue 2 (7th September 2017)

• Record Type: Journal Article
• Authors: Du, Junfeng; Chi, Yumin; Song, Zhan; Di, Qingguo; Mai, Zhitao; Shi, Jian; Li, Min
• Is Part Of: Journal of cellular biochemistry. Volume 119:Issue 2(2018)
• Page Start: 1746
• Page End: 1754
• Publication Date: 2017-09-07
• Subjects: Aspergillus fumigatus -- chronic obstructive pulmonary disease -- crocin -- inflammation -- NF‐κB; Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.26335
• Languages: English
• ISSNs: 0730-2312

Abstract

Abstract: Chronic obstructive pulmonary disease (COPD) is a chronic airway inflammation and its exacerbation is often accompanied by Aspergillus fumigatus (A. fumigatus) infection. Increasing evidences demonstrated the potent antioxidant and ‐inflammatory effects of crocin. However, the role of crocin in A. fumigatus ‐induced inflammation is still unknown. We aimed to evaluate the role of crocin in inflammation response induced by A. fumigatus in human bronchial epithelial cells and the possible mechanisms. BEAS‐2B and NHBE cells were pretreated with crocin for 24 h, and then A. fumigatus conidia were added for 24 h. A. fumigatus treatment exhibited a significant higher TNF‐α, IL‐8, IL‐6, and IL‐1β level ( P < 0.05), whereas crocin pretreatment significantly inhibited A. fumigatus induced the pro‐inflammatory cytokines ( P < 0.05). NF‐κB inhibitor PDTC inhibited pro‐inflammatory cytokines release triggered by A. fumigatus ( P < 0.05). Furthermore, crocin suppressed A. fumigatus induced NF‐κB p65 nuclear translocation, the phosphorylation of IKKα and IκBα, the degradation of IκBα and NF‐κB reporter activity. Crocin pretreatment also resulted in an inhibition of A.fumigatus ‐induced ROS production ( P < 0.05). Taken together, these results indicate that crocin may prevent A. fumigatus ‐induced inflammation through suppressing NF‐κB signal pathway. Abstract : These results indicate that crocin may prevents A. fumigatus ‐induced inflammation through suppressing NF‐κB signal pathway.