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The Impact Of Anxiety And Depression On The Airway Hyperresponsiveness And Inflammation In Asthmatic Mice

Posted on:2015-12-30Degree:MasterType:Thesis
Country:ChinaCandidate:T C JiangFull Text:PDF
GTID:2284330431996504Subject:Internal medicine
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BackgroundBronchial asthma is a common chronic diseases, in addition to causingdiscomfort on the body, the asthma patients can easily combined with anxiety anddepression, seriously affect the asthma control and quality of life, showed a "viciouscycle", therefore asthma is also considered a psychosomatic disorders. However,given anxiolytic, antidepressant treatment to the asthma patients combined withanxiety and depression is not sufficient awareness, especially the effects of anxietyand depression on airway hyperresponsiveness and airway inflammation in asthmahas not been reported.PurposeThe asthma, anxiety and depression model were established by BALB/c mice,from these models to study the affect of anxiety and depression on the airwayhyperresponsiveness and airway inflammation. Meanwhile study the effects ofanxiolytic and antidepressant on the airway hyperresponsiveness and airwayinflammation. From these studies we want to supply laboratory basis for anxiolyticand antidepressant therapy used in asthma combined anxiety and depression patients. MethodNinety BALB/c mice were randomly divided into control group, asthma group,anxiety group, depression group, asthma treatment group, asthma anxiety group,asthma anxiety treatment group, asthma depression group, asthma depressiontreatment group(ten in each group). The ovalbumin-induced method was used tobuilt asthma model in asthma group, asthma treatment group, asthma anxiety andasthma depression group, the uncertainty bottles of drinking water method was usedto establish anxiety models and the chronic mild unpredictable stimuli methed wasused to built depression model. At the last week, the escitalopram was used in sthmatreatment group, asthma anxiety treatment and asthma depression treated group byintraperitoneal injections, the other groups were received an equal volume ofphosphate buffer. The control group mice were normal feeding ad libitum intake ofwater, inhalation and intraperitoneal injection with the same volume of phosphatebuffer. The elevated plus maze and forced swim methods were used to assess thelevels of anxiety and depression, non-invasive method to detect the mouse airwayreactivity, recovery bronchoalveolar lavage fluid of mice in each group counts andcytological bronchoalveolar lavage lotion inflammatory factors.Results1.The anxiety and depression levels increasing after the models induced by OVAthan in the control group (all P <0.05); the levels of anxiety in asthma anxiety groupwere higher than in the asthma group(P <0.05), the levels of depression in asthmadepression group were higher than in the asthma group (P <0.05); the levels ofanxiety and depression in asthma treatment group were lower than in the asthmagroup(P <0.05), the levels of anxiety in asthma anxiety treatment group were lowerthan in the asthma anxiety group(P <0.05), the levels of depression in asthmadepression treatment group were lower than in the asthma depression group (P<0.05).2. Asthma, anxiety and depression can increase airway hyperresponsiveness (allP <0.05); the airway hyperresponsiveness in asthma anxiety group and asthma depression group were higher than in the asthma group(all P <0.05); the airwayhyperresponsiveness in asthma treatment group were lower than in the asthmagroup(all P <0.05); the airway hyperresponsiveness in asthma anxiety treatmentgroup were lower than in the asthma anxiety group(all P <0.05); the airwayhyperresponsiveness in asthma depression treatment group were lower than in theasthma depression group(all P <0.05).3. After the models induced by OVA,the total number of inflammatory cells,percentage of eosinophils, and the levels of IL-4, IL-13in the bronchoalveolar lavagefluid were higher than those in the other groups (all P <0.05). The total number ofinflammatory cells, percentage of eosinophils, and the levels of IL-4, IL-13in thebronchoalveolar lavage fluid of asthma anxiety group and asthma depression groupwere higher than in the asthma group(all P <0.05). Compared with the control group,the total number of inflammatory cells, percentage of eosinophils, and the levels ofIL-4, IL-13in the bronchoalveolar lavage fluid of the anxiety and depression grouphave no significant difference (all P>0.05). In the asthma treatment group the totalnumber of inflammatory cells, percentage of eosinophils, and the levels of IL-4,IL-13in bronchoalveolar lavage fluid were lower than these in asthma group (allP<0.05). In the asthma anxiety treatment group the total number of inflammatorycells, percentage of eosinophils, and the levels of IL-4, IL-13in bronchoalveolarlavage fluid were lower than these in asthma anxiety group (all P<0.05).In theasthma depression treatment group the total number of inflammatory cells, percentageof eosinophils, and the levels of IL-4, IL-13in bronchoalveolar lavage fluid werelower than these in asthma depression group (all P<0.05). Successfully constructedBALB/c mice were anxiety, depression model in this studyConclusion1. The anxiety and depression model can be built sucessfully by BALB/c mousein this study;2. Anxiety and depression can increase the airway hyperresponsiveness andinflammation 3. Anxiolytic and antidepressant therapy have a benefit for the control of asthmaairway hyperresponsiveness and inflammation.
Keywords/Search Tags:Asthma, Anxiety, Depression, Airway hyperresponsiveness, Airwayinflammation, Mice
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