| Chronic obstructive pulmonary disease is a disease with limited airflow characteristics and its pathological basis for airway wall and chronic inflammation of the lung parenchyma and structural damage. In the development of COPD, the long-term repeated inflammation may eventually cause pulmonary fibrosis.Chronic obstructive pulmonary diseases combined with pulmonary interstitial fibrosis (PIF-COPD) is the inevitable trend in the progress of COPD and pathological outcomes.1. PIF-COPD model and evaluation indexObjective:To determine the PIF-COPD animal model and testing index.Methods:The rat trachea driping BLM6mg/kg superposition cigarette smoke stimulating47days builded PIF-COPD animal model. By detecting lung function, lung index and lung tissue pathology, Sirius red staining to observe the change of collagen Ⅰ and Ⅲ, protein microarray chip to detect the serum cytokine expression, evaluation model is or not in line with the PIF-COPD pathologic physiology characteristic.Results:(1) The results of respiratory function test showed:model group rats center airway resistance, organizing damping, dynamic elastic increased significantly, and the cdyn decreased significantly compared with control group (P<0.05).(2) The results of lung index showed:compared with normal group, model group rats lung index increased significantly (P<0.05).(3) The pathological tests revealed:model group rats of lung tissue characterized inflammatory infiltrates, type Ⅰand Ⅲ collagen content increased significantly, and the rats showed the emphysema, fibrosis pathological manifestations.(4) Serum test resulted:the model group rats’the serum levels of MMP-8, TIMP-1, IL-10, IL-13, PDGF-AA and Beta-NGF increased obviously, RAGE reducing compared with control group (P<0.05).Conclusion:Rat trachea dripping BLM6mg/kg superposition cigarette smoke stimulated47days can be used as PIF-COPD animal model; Detection of respiratory function, the serum levels of MMP-8, TTMP-1, IL-13, PDGF-AA and NGF canplay as the evaluation indicators of the model.2. The FFKXJN intervention effect of PIF-COPD model ratsObjective:To study the FFKXJN intervention effect of PIF-COPD animal model and mechanism of action.Methods:The rat trachea driping BLM6mg/kg superposition cigarette smoke stimulation47days builded PIF-COPD animal model. FFKXJN doses were0.35,0.70,1.4g/kg. After building PIF-COPD animal model32days, rats had been begun to gavage administration for39days. Detecting lung function, lung tissue pathology detection, Sirius red staining to observe the lung tissue collagen distribution, ELISA method to detect the serum IL-6, IL-8, IL-10, IL-13, GM-CSF, SICAM-1, TGF-β1, NE, TNF-α, ET-1, L-Selectin, TMP-1, MMP-9, al-AT content, immunohistochemical method to detect lung tissue expression of α-AT, MM-9and TTMP-1, NGF and PDGF-AA. Results:(1) The result of respiratory function test showed that FFKXJN each dose group could restrain model rats increased airway resistance and lung compliance in different degree. Thereinto, FFKXJN1.4g/kg could obviously inhibit the model of rat cdyn decreased compared with model group (P<0.05); Each dose group of FFKXJN could restrain model rats of choline acetyl methyl chloride reaction degree in different degree. Thereinto, FFKXJN1.4g/kg could obviously restrain model rats with airway resistance increased by caused acetylcholine chloride0.625,1.25mg/mL; FFKXJN0.35g/kg could obviously restrain model rats with airway resistance increased by caused acetylcholine chloride1.25mg/mL compared with model group (P<0.05).(2) Serum test result showed:FFKXJN doses could be different degree of inhibition of model rats increased serum levels of inflammatory cytokines. Thereinto FFKXJN doses could obviously restrain Model rats increased serum levels of TNF-a, ET-1, TGF-131.FFKXJN0.70,1.4g/kg could obviously restrain model rats increased serum levels of EL-6, SICAM-1, GM-CSF. FFKXJN1.4g/kg could obviously restrain model rats increased serum levels of IL-8, JL-13(P<0.01). FFKXJN0.70,1.4g/kg could obviously restrain model rats model rats increased serum levels of HYP (P<0.01). Moreover, FFKXJN doses could obviously restrain model rats increased serum levels of TTMP-1, MMP-9,NE and al-AT(P<0.01). FFKXJN doses also obviously inhibited the increase of MDA content and SOD activity decreased (P<0.01).(3) Immunohistochemical method test results showed: FFKXJN doses could obviously inhibit model rats α1-AT,MMP-9and TIMP-1, PDGE-AA and NGF increased expression in the trachea and lung interstitial (P<0.05, P<0.01).(4) Sirius red staining results showed, FFKXJN doses could obviously restrain model rats type I collagen content increased significantly (P<0.01).Conclusion:FFKXJN could reduce airway obstruction, cdyn and slow PIF-COPD rat pathological change through adjusting anti-inflammatory, protease/anti-prosease imbalances and antioxidation. |
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