crocin and prolinedithiocarbamate

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.

Topics: Anti-Inflammatory Agents; Aspergillus fumigatus; Carotenoids; Cell Line; Epithelial Cells; Humans; I-kappa B Kinase; Models, Biological; NF-kappa B; NF-KappaB Inhibitor alpha; Proline; Pulmonary Disease, Chronic Obstructive; Signal Transduction; Thiocarbamates; Transcription Factor RelA