Effect Of RSV-induced Autophagy Of Dendritic Cells On Airway Responsiveness In Asthmatic Mice And The Intervention Of Wuhu Decoction

Objective: To observe the effect of RSV-induced DC autophagy on airway responsiveness in asthmatic mice,and to provide evidence for the role of RSV-induced DC autophagy in the development of asthmatic "Fuxi";observe Wuhu Decoction for RSV-induced asthma The improvement of airway hyperresponsiveness in the murine model provides a basis for further elucidating the mechanism of action of Wuhu Decoction from the regulation of autophagy.Methods:(1)Airway responsiveness and pathological findings of lung tissue indicate that the RSV-induced asthma mouse model was successfully established.(2)When the concentration of methacholine was 7.25,12.5,25,50 ? g/ml,the R1 value of asthma group was significantly higher than that of normal group(P<0.01),Wuhu decoction group,dexamethasone group,rapamycin.The RL value of the mice in the group was significantly lower than that in the asthma group(P<0.01).(3)AB-PAS staining showed that PAS staining positive cells were almost invisible in the normal group,and PAS staining positive cells were significantly increased in the asthma group;compared with the normal group,the airway mucus reserve index of the asthma group was significantly increased(P<0.01).(4)Transmission electron microscopy and Western Blot results showed that the relative expressions of LC3 I,LC3II and Beclin-1 in lung tissue of asthmatic mice were significantly increased(P<0.01).Compared with asthma group,Wuhutang low,medium and high doses The levels of LC3II/LC3 I in the rapamycin group were significantly increased(P<0.01),and the levels of Beclin-1 were also significantly up-regulated(P<0.05).The levels of LC3II/LC3 I and Beclin-1 were compared in the dexamethasone group compared with the asthma group.There was no statistical difference in expression.Results:(1)Airway responsiveness and pathological findings of lung tissue indicate that the RSV-induced asthma mouse model was successfully established.(2)When the concentration of methacholine was 7.25,12.5,25,50?g/ml,the R1 value of asthma group was significantly higher than that of normal group,the difference was statistically significant(P<0.01).Wuhu decoction group and ground The RL value of dexamethasone group and rapamycin group was significantly lower than that of asthma group,and the difference was statistically significant(P<0.01).(3)AB-PAS staining showed that PAS staining positive cells were almost invisible in the normal group,and PAS staining positive cells were significantly increased in the asthma group.Compared with the normal group,the airway mucus reserve index of the asthma group was significantly increased,and the difference was significant.Statistical significance(P <0.01).(4)Transmission electron microscopy and Western Blot results showed that the relative expressions of LC3 I,LC3II and Beclin-1 in lung tissue of asthmatic mice were significantly increased(P<0.01).Compared with asthma group,Wuhutang low,medium and high doses The levels of LC3II/LC3 I in the rapamycin group were significantly increased,the difference was statistically significant(P<0.01),and the Beclin-1 level was also significantly up-regulated.The difference was statistically significant(P<0.05).The dexamethasone group Compared with the asthma group,the relative expressions of LC3II/LC3 I and Beclin-1 were not statistically different(P>0.05).Conclusion:(1)RSV can induce the increase of autophagy level of DC cells in lung tissue of asthmatic mice.(2)Up-regulation of RSV-induced autophagy in lung dendritic cells can reduce asthmatic airway responsiveness.(3)Wuhu Decoction can effectively reduce airway hyperresponsiveness in RSV-induced asthmatic mice.(4)Wuhu Decoction can significantly increase the level of autophagy in dendritic cells of RSV-induced asthmatic mice in lung tissue.(5)The effect of Wuhu Decoction on improving airway hyperresponsiveness in RSV-induced asthmatic mice may be related to the up-regulation of autophagy in dendritic cells in asthmatic mice.