Effects of catalpol on asthma by airway remodeling via inhibiting TGF-beta 1 and EGF in ovalbumin-induced asthmatic mice

Airway remodeling represents the healing and alteration in the airway that occur as a consequence of chronic inflammation. Extracellular matrix synthesis regulated by transforming growth factor (TGF-beta 1) and vascular remodeling regulated by epidermal growth factor (EGF) are important factors for the airway remodeling. This study aimed to probe the effect of catalpol, a major component of Radix Rehmanniae Preparata (Shudihuang), on airway remodeling and expression of TGF-beta 1 and EGF in asthmatic mice. A mice model of asthma was induced by ovalbumin (OVA) treatment. BALB/c mice were randomly divided into blank control group, asthma model group, dexamethasone (DEX) group (positive control), high, medium and low dose of catalpol intervention group. Changes in lung histology were observed using hematoxylin and eosin staining. The levels of TGF-beta 1 and EGF in mouse sera and bronchoalveolar lavage fluid (BALF) were examined by ELISA. The EGF mRNA and protein levels in mice tissues were determined. The results indicated that catalpol improved general conditions and reduced the damage of lung tissues in asthmatic mice. Moreover, results of ELISA revealed that catalpol significantly reduced the OVA-induced levels of TGF-beta 1 and EGF in sera and in bronchoalveolar lavage fluid (BALF). Additionally, results indicated that catalpol decreased the OVA-induced EGF mRNA and protein expression in lung tissues in asthmatic mice. Catalpol at a high dose was more efficient in decreasing the level of TGF-beta 1 in mice sera and BALF comparing the DEX group. Current study has demonstrated that catalpol might effectively prevent airway remodeling in asthma via inhibiting TGF-beta 1 and EGF.