Study On The Mechanism Of CyclinD1 And E In Airway Remodeling Of COPD Rats And The Intervention Of Fufang Xueshuantong Capsule

Objective:This subject adopts the method of smoked in rats COPD model,selection of Chinese medicine compound thrombosis with blood circulation function of capsule intervention related changes by morphological changes and CyclinD1,Cyclin E were observed before and after the lung tissue of rats in mRNA level and protein expression,effect of CyclinD1,Cyclin E COPD in the airway remodeling mechanism and activating blood circulation method on airway remodeling of COPD rat model,study the mechanism of prevention may retard or improve airway remodeling in COPD disease process,provide a theoretical basis for clinical application of Fufang Xueshuantong capsule in the prevention and treatment of airway remodeling in COPD.Method:1.To establish the COPD rat model: the rat model of COPD was successfully prepared by repeated smoking;2.Drugs by gavage in rats,prepared the pathological section of lung tissue was observed after peripheral tissue morphological changes related to bronchi and vessels of rat lung tissues and statistical analysis;reverse transcription polymerase chain reaction(Revers trnaseription polymerase chain reaction,RT-PCR),enzyme-linked immunosorbent assay,immunohistochemistry,detection CyclinD1,CyclinE in the level of mRNA and protein expression and statistical analysis.Result:1.Behavioral changeCOPD model rats with varying degrees of shortness of breath,mouth and nose secretions increase,irritability,dry hair,tired,and real activity significantly reduced or even,shortness ofbreath,abdominal muscle twitching,wheezing and other symptoms,show that the model successfully.The prednisone group,Fufang Xueshuantong high middle and low dose intervention rats symptoms and signs were alleviated,the high dose group significantly reduced but still Biponisong group,normal control group showed no abnormalchanges.2.Pathological findings of lungThe lung tissue of rats left,HEstaining: the bronchial epithelium in rats of model group COPD off,goblet cells increased,and the pipe wall around the infiltration of inflammatory cells;alveolar structure disorder,disruption of alveolar wall,alveolar fusion,formation of pulmonary bullae;collagen fibers,small airway collagen fiber thickening.The proliferation of smooth muscle cells,arranged a little messy,smooth muscle layer thickening,lumen narrowing and vascular wall thickening,the above were consistent with the pathological manifestations of COPD,suggesting that the model was successful.The prednisone group,Fufang Xueshuantong high middle and low dose intervention rats pathological results were alleviated,the high dose group significantly reduced but still Biponisong group,normal rats bronchial and alveolar structure clear,collagen fibers increased obviously.3.Expression of CyclinD1,CyclinE in lung tissue of ratsCompared with normal group,significantly up-regulated CyclinD1,CyclinE expression in lung tissue of rats in COPD model group;prednisone,the Fufang Xueshuantong capsule can level CyclinD1,Cyclin E expression in lung tissue of rats with lower,compared with the model group(P < 0.05),the high dose group was down regulated but is still lower than the prednisone group.Conclusion:1.CyclinD1,Cyclin E expression in rats increased significantly,and the degree of airway remodeling(bronchial smooth musecle thickness)was positively related to speculate in the process of forming the airway remodeling of COPD,CyclinD1,Cyclin E play an important role;2.Fufang Xueshuantong capsule can improve the airway inflammation and airway inflammatory cell infiltration in lung tissue of rats with airway remodeling;3.Fufang Xueshuantong capsule can reduce the expression of CyclinD1 and Cyclin E in the lung tissue of rats with COPD airway remodeling,degrade the synthesis of collagen,decrease the proliferation of airway smooth muscle and slow down the COPD airway remodeling;4.Traditional Chinese medicine Huoxue Huayu method can reduce the expression of CyclinD1,Cyclin E,which is the key factor of airway remodeling by promoting blood circulation,so as to prevent the airway smooth muscle cells and the pathological hyperplasia of collagen,and interfere with the airway remodeling of COPD.