| Research background:chronic bronchitis is a disease that the etiological factor and pathogenesis are not understood entirely,endangering seriously the health of elderly patients,and it is a preventable,treatable disease currently. Smoking is one of the marjor risk factors for the development of chronic bronchitis besides dust,irritating,gases ,infection,immunication,age,climate.It has been applied successfully that replicated animal model of chronic bronchitis with smoking. High mobility group box-1 protein is a highly conserved prevalent nuclear protein ,it participates in DNA transcription, replication, repairment and inflammatory reactions. It is found that a certain level of HMGB1 expressed in both the human and rat airways . HMGB1 plays an important role in maintaining the normal function of the respiratory system. HMGB1 has a role of proinflammatory cytokines in lung tissue,it mediated important acute lung inflammation biological mediator. As a late inflammatory cytokines,HMGB1 playes an important regulatory role of inflammation,There have been many research reports of HMGB1 in lung injury, lung cancer, pulmonary fibrosis and other lung diseases, but few on COPD . However,there is no report on the role of HMGB1 in chronic bronchitis. This study established a rat model of human chronic bronchitis with smoking and detected the HMGB1 expression ,discussing the role of HMGB1 in chronic bronchitis.Objective:By establishing the rat model of chronic bronchitis, detecting rat model expression of HMGB1 in lung tissue and serum and comparing the expression of HMGB1 between the model group and the control group to reveal the role of HMGB1 of chronic bronchitis in rat model induced by smoking.Methods:The male SD rats were randomly divided into normal control group and smoking model group, 14 rats in each group. Model rats were placed inside the homemade sealed box for passive smoking,smoking 2 times a day with an interval longer than 4 h, 14 sigerates each time for 30 minutes,the concentration of smog is about 5% (v / v), Six days per week,continuously for 75 days. The lung tissue section stained by HE was observed under optical microscope in order to study the alternation of histopathologic.Total cell counts and differential analysis in BALF were performed.The concentrations of HMGB1 in serum were detected by ELISA,The expression of HMGB1 in the lung tissue was detected by immunohistochemical method .Results:The athological changes in smoking model group were consistent with that of chronic bronchitis.The total cell counting, mononuclear macrophage and neutrophil percentage In BALF were 5.12±0.69×108/L,69.62±4.82%,22.62±2.47%;1.79±0.19×108/L,86.00±2.45%,7.71±1.27% in two groups respectively with significant differences between the smoking model group and normal control group ( P < 0.05). The concentrations of HMGB1 in serum were 2.41±0.31 ug/L,1.60±0.16 ug/L in model group and normal control group respectively indicating that HMGB1 in the model group significantly increased compared with the control group (P <0.05). HMGB1 was found in the bronchial and alveolar epithelial cells , it increased significantly tban that the expression intensity of HMGB1 in model group lung tissue,using graphical analysis software to analysis of staining results, measuring and recording the positive staining of HMGB1 per field, the average integrated optical density (IOD) of the model group and the control,the expressions of HMGB1 in the lungs was obviously elevated in the model group(P <0.05).Conclusions:1. The concentrations of HMGB1 in serum in the model group significantly increased as compared with the control group.2. HMGB1 was found in the bronchial and alveolar epithelial cells, compared with the control group, the expressions of HMGB1 in the lungs was obviously elevated in the model group.3. The expressions of HMGB1 in the lungs and the concentrations of HMGB1 in serum in the model group significantly increased as compared with the control group,the results were statistically significant,HMGB1 may play a role in the pathogenesis of chronic bronchitis,but the exact mechanism needs further investigation. |
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