Club Cell Secretion Protein 16 (CC16) Improve Chronic Obstructive Pulmonary Disease In Vivo Study

Purpose: The purpose of this study was to evaluate CC16 in COPD treatment and relative mechanism by vivo study. Materials and methods: The mice were divided into Normal, Model and CC16 groups. Measuring Pathology and goblet cell number by HE or AB/PAS staining; Evaluating apoptosis cell number by TUNEL assay; using flow separation to analysis inflammatory cells in difference groups; MAPK and NF-kappa B(p65) protein expression were evaluated by IHC assay in tissues; Total protein concentration of MUC5AC, CC16, Bax and Bcl-2 were evaluated by Western Blot (WB) assay. Results: Compared with Normal group, the pathology was deteriorate and goblet cell number were significantly up-regulation in Model group, apoptosis goblet cell number were significantly depressed (P < 0.001), lympbocyte rate and hypertrophic rate were significantly down-regulation and Eosinophils rate, Macrophage rate and Neutrophils rate were significantly up-regulation (P < 0.001, respectively) in Model group. By IHC assay, MAPK and NF-kappa B(p65) proteins expression were significantly increased (P < 0.001, respectively) in Model group; by WB assay, MUC5AC and Bcl-2 protein expression weresignificantly up-regulation and CC16 and Bax proteins expression were significantly down-regulation (P < 0.001, respectively) in Model group. CC16 supplement, the COPD were significantly improved with relative inflammatory cells rates significantly improving and relative proteins improving. Conclusion: CC16 could improve COPD by inducing goblet cell apoptosis increasing via regulation MAPK/NF-kappa B(p65) pathway in vivo study.