Abstract

Objective: The aim of our research was to evaluate Nrf2 in COPD treatment and relative mechanism by vivo study.Materials: The mice were divided into Normal, Model and CCL16 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-κB(p65) protein expression were evaluated by IHC assay in tissues; Total protein concentration of MUC5AC, Nrf2, Bax and Bcl-2 were evaluated by 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-κB(p65) proteins expression significantly increased (P< 0.001, respectively) in Model group; by WB assay, MUC5AC and Bcl-2 protein expression were significantly up-regulation and Nrf2 and Bax proteins expression were significantly down-regulation (P< 0.001, respectively) in Model group. Nrf2 supplement, the COPD were significantly improved with relative inflammatory cells rates significantly improving and relative proteins improving.Conclusion: Nrf2 could improve COPD by inducing goblet cell apoptosis increasing via regulation MAPK/NF-κB(p65) pathwayin vivostudy.

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