Abstract
Hedyotis diffusa Willd (HDW) is a constituent of several Chinese medicines used clinically to treat inflammatory diseases, including airway inflammation. The aim of the present study was to investigate whether HDW serves a protective role in suppressing chronic airway inflammation and its underlying mechanisms. A mouse model of chronic smoking was induced via exposure to cigarette smoke (CS) for 30 days, increasing the exposure time for up to 5 min per day and the administration of lipopolysaccharide (LPS). Mice were gavaged with HDW (50 or 100 mg/kg body weight), dexamethasone (1 mg/kg body weight) or normal saline (NS, 0.9%) 1 h prior to CS challenge. Compared with CS and LPS (SL)-induced mice, the levels of interleukin (IL)-1β, tumor necrosis factor-α and transforming growth factor-β in bronchoalveolar lavage fluid from HDW+SL mice were significantly decreased and IL-10 was markedly reduced. Histological examination of the lung tissues revealed that HDW treatment alleviates airway inflammation. In addition, the administration of HDW to human bronchial epithelial BEAS-2B cells suppressed the activity of the nuclear factor (NF)-κB signaling pathway. The results of the present study demonstrate that HDW has a therapeutic effect in COPD and the underlying mechanism may be attributed to inhibition of the NF-κB pathway.