Hydroxysafflor yellow A attenuates allergic airway inflammation by suppressing the activity of nuclear factor-kappa B in ovalbumin-induced asthmatic mice

Objective: This study is to investigate the effects of hydroxysafflor yellow A (HSYA) on the airway inflammation in ovalbumin (OVA)-induced asthmatic mice. Methods: After drug administration, the airway hyper-responsiveness (AHR), and cell differentials and cytokine levels in bronchoalveolar lavage (BAL) fluid, were assessed. Lung tissue was detected with histological examination. Protein expression levels were determined with Western blot analysis. NF-κB/DNA binding activity was assessed with the electrophoretic mobility shift assay (EMSA). Results: The AHR, cell chemotaxis, and inflammatory responses were substantially enhanced in OVA-induced asthmatic mice, which would be prevented by HSYA or BAY 11-7085. Moreover, levels of total and OVA-specific IgE, and inflammation-related cytokines, in the BAL fluid were significantly increased in OVA-induced asthmatic mice, which would be decreased by HSYA or BAY 11-7085. On the other hand, the nuclear NF-κB p65 level was significantly increased, while the cytosolic NF-κB p65 level was significantly decreased, by the OVA challenge. Moreover, EMSA showed increased NF-κB/DNA binding activity in OVA-induced asthmatic mice. Furthermore, immunostaining confirmed the nuclear translocation of the p65 subunit. However, the treatment of HSYA or BAY 11-7085 significantly inhibited the nuclear translocation of NF-κB p65 in OVA-induced asthmatic mice. In addition, the treatment of HSYA or BAY 11-7085 significantly reduced the phosphorylation and degradation of IκB-α in lung of OVA-induced asthmatic mice. Conclusion: HSYA protects against the airway inflammation in OVA-induced asthmatic mice, through down-regulating inflammation-related cytokines and inhibiting NF-κB activity. Our findings support the utility of HSYA in the treatment of asthma in clinic.