Berberine attenuates cigarette smoke-induced airway inflammation and mucus hypersecretion in mice

Cigarette smoke-induced airway inflammationmucus over-production is one of the most important pathogenic features of chronic airway diseases. This study aimed to investigate the effect of berberine, a plant alkaloid with strong anti-inflammatory property, on cigarette smoke-induced airway inflammation and mucushypersecretion in mice. Mice with exposure to cigarette smoke wereintraperitonealy injected with berberin (5, 10 mg/kg.d). Inflammatory cytokines TNF-alpha, IL-1 beta and MCP-1 levels in bronchoalveolar lavage fluid were determined by ELISA. Lung tissue was examined for histopathological lesions and goblet cell hyperplasia. The expression of signaling proteins in lung tissue, ERK and P38 were detected using Western Blot. Cigarette smoke exposure significantly increased the release of inflammatory cytokines TNF-alpha, IL-1 beta, MCP-1 and inflammatory cells in bronchoalveolar lavage fluid, and it also induced goblet cell hyperplasiaand the expression of mucin-5ac in the airway of mice. Pretreatment of berberineinhibited cigarette smoke-induced airway inflammation and mucus production. Cigarette smoke exposure also increased the expression of ERK and P38, meanwhile, berberineintervention can inhibit such changes. In summary, berberine inhibits cigarette smoke exposure-induced airway inflammation and mucus hypersecretion in mice, which may partly act through inhibition of ERK and P38.