Chrysophanol attenuates airway inflammation and remodeling through nuclear factor-kappa B signaling pathway in asthma

Chrysophanol (CHR), a purified active constituent extracted from Rheum palmatum L., possesses anti-inflammatory activity. This study aimed to evaluate its effects on asthma-associated airway inflammation and remodeling. BALB/c mice were sensitized and challenged by ovalbumin (OVA) and administrated with different doses of CHR. We found that CHR decreased OVA-induced pulmonary inflammation: the levels of interleukin (IL)-4, IL-5, and IL-13, tumor necrosis factor (TNF)-alpha, and inducible nitric oxide synthase were downregulated. CHR also attenuated airway remodeling induced by OVA challenge-CHR inhibited pulmonary alpha-smooth muscle actin expression. Moreover, both the nuclear translocation and activity of NF-kappa B p65 were inhibited by CHR in the asthmatic lung. Enhanced autophagy was initiated in the lung by OVA challenge as evidenced by upregulated light chain 3 beta, autophagy-related protein 5, and Beclin 1. CHR suppressed OVA-induced alterations in these autophagy-related molecules. In vitro, CHR (2 or 20 mu M) was used to treat human pulmonary epithelial BEAS-2B cells in the presence of 10 ng/ml recombinant TNF-alpha. CHR not only exhibited the antiproliferation effect but also inhibited the activation of nuclear factor-kappa B (NF-kB) signaling pathway in TNF-alpha-treated BEAS-2B cells. In conclusion, our study indicates that CHR has the potential to ameliorate asthma.