| Objective: The rat model of chronic asthma was established by ovalbumin sensitization and ovalbumin atomization challenge.Pingchuanning prescription was used to interfere with cold asthma rats to observe its effect on airway inflammation,and to explore the effect of Pingchuanning on the production of corresponding proteins in PI3K-Akt/PKB signal pathway,and then to study the mechanism of Pingchuanning prescription in delaying airway remodeling of asthma.Methods: 105 male healthy clean grade SD rats aged about 6 weeks were randomly divided into seven groups: normal group,model group,high,middle and low dose of Pingchuanning group,Guilong Kechuanning group and dexamethasone group,with 15 rats in each group.On the 1st and 8th day after adaptive feeding,the rats in six groups of asthma were sensitized by intraperitoneal injection of 1ml and 10% ovalbumin(which was formed by the dissolution of OVA and normal saline at 10% concentration).On the 15 th day,the rats were stimulated by 1%OVA ultrasonic atomization,30 minutes each time,once a day;at the same time,the rats were placed in a cold box with controllable temperature(0-2 ?)for 2 hours each time,once a day for 7 days.The rats in the blank control group referred to the above methods,but normal saline was used instead of OVA during sensitization and challenge.After the rat model of cold asthma was successfully established,from the 22 nd day on,the corresponding drugs were given to the rats by intragastric administration according to the adult dose,once a day for 28 days.In the process of modeling,the general changes of rats were observed,and the body weight and death were recorded.After the intervention,the pathological changes such as inflammatory cell infiltration and smooth muscle changes in lung tissue sections were observed by HE staining,and the expression of p110,PTEN and PIP3 protein in lung tissue was detected by Western blot method,and the expression of PDK1 and GSK3 in lung tissue was detected by immunohistochemical method.Results:1.Pathological changes of lung tissue in each group: in the normal group,the airway structure of lung tissue was intact,the bronchial lumen was smooth,there was no obvious infiltration of inflammatory cells in airway and surrounding vascular tissue,and the morphology and structure of smooth muscle was normal.The results of lung histopathology in Pingchuanning group and dexamethasone group were lighter than those in model group,the structure of lung tissue was more complete,a small amount of inflammatory cell infiltration could be seen around,bronchial contracture was less,there was no thickening of smooth muscle,and the bronchial lumen was close to normal.There was also pathological improvement in Guilong Kechuanning group,but lower than that in dexamethasone group.2.The expression of PDK1 in lung tissue of rats in the model group was significantly higher than that in the normal group,while the expression of GSK 3?in the model group was significantly lower than that in the normal group(P < 0.01).Compared with the model group,the expression of PDK1 in the high and middle dose of Pingchuanning groups decreased significantly,while the expression of GSK 3? increased significantly(P < 0.01).3.Compared with the normal group,the expression of p110?protein and PIP3 protein in the lung tissue of the model group was significantly increased(P < 0.01),and the expression of PTEN protein was significantly decreased(P<0.01).Compared with the model group,the expression of p110? protein and PIP3 protein in the lung tissue of rats in the high and middle dose of Pingchuanning groups was significantly down-regulated(P< 0.01).The expression of PIP3 protein was up-regulated(P < 0.01).Conclusion:1.Pingchuanning can reduce the infiltration of inflammatory cells in the bronchus and periphery of asthmatic rats,repair the destruction of the vessel wall,reduce the mucus thrombus in the lumen,improve the proliferation of bronchial smooth muscle,and alleviate the thickening of the bronchial wall.Airway stenosis was also improved.2.Pingchuanning can relieve airway inflammation and airway remodeling by regulating GSK3,PDK1,p110,PTEN and PIP3,in PI3K-Akt signal transduction pathway. |
PDF Full Text Request