Calpeptin attenuates cigarette smoke-induced pulmonary inflammation via suppressing calpain/IκBα signaling in mice and BEAS-2B cells

Exposure to cigarette smoke including secondhand smoking is the most important risk factor in the development of chronic obstructive pulmonary disease where incidence has substantially increased in recent decades. The mechanisms responsible for cigarette smoke-induced pulmonary inflammation remain unclear, and thus lack of effective treatment. The present study investigated the effect of calpeptin on attenuating cigarette smoke induced pulmonary inflammation and its potential mechanism and function. When BALB/c mice were exposed to cigarette smoke and received calpeptin intraperitoneally injection after 90 days, calpeptin histologically attenuated the accumulation of neutrophils (P < 0.001), eosinophils (P < 0.001), macrophages (P < 0.01), fibrinous exudation and proliferation within the interstitial and alveolar spaces. BEAS-2B cells were added with cigarette smoke extract in vitro and treated with calpeptin for 24h in the treatment group. The markedly up regulation of-calpain (P < 0.01), m-calpain (P < 0.001) and I kappa B alpha (P < 0.01) in cigarette smoke-induced lungs were simultaneously decreased by calpeptin treatment (P < 0.05). The increased expression of-calpain, m-calpain and I kappa B alpha (P < 0.05) in cigarette smoke extract-stimulated BEAS-2B cells were also decreased by calpeptin treatment (P < 0.05). These data indicated that calpeptin attenuated cigarette smoke-induced pulmonary inflammation by suppressing the pathway of p-calpain, m-calpain and I kappa B alpha in vivo and in vitro. Calpeptin might have a potential for prevention of the development of inflammatory pulmonary diseases and warrant further pharmaceutical investigation.