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Atrial Natriuretic Peptide(ANP) Signaling In The Pathogenesis Of Asthma And The Mechanism

Posted on:2016-10-13Degree:MasterType:Thesis
Country:ChinaCandidate:Y GaoFull Text:PDF
GTID:2284330464452405Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective: To discussed the effects of atrial natriuretic peptide signaling pathway on the bronchial asthma pathogenesis in mice.Methods : 40 BALB/C mice which is clean and female, random divided into normal group, Asthma model group, the anp and the anp inhibitor group,each group contains 10. To established mice models of asthma and ANP intervention;Using the method of ELISA to measure the type Th1 cytokines IFN- gamma and Th2 cytokines IL-4 levels in BALF of mice,To observed the change of airway inflammatory and mucus secretion of each group by Lung tissue pathology. Using immunohistochemistry technique to detect the expression of T-bet and GATA-3protein in lung tissue of each models. Using Western blotting test(WB) to detected the expression of NPRA、T-bet and GATA-3 protein in lung tissue of each models.Results:1.The behavior change of mice model were established : besides the normal mice,other groups of mice all have different degrees of behavior change, such as scratching their heads, restlessness, shortness of breath and even incontinence.2.To Observe the lung tissue pathology in mice: compared with normal group model mice, the mice in group BA showed the situation of bronchial mucosal hyperemia and edema and tracheal inflammatory cell infiltration was significantly(P<0.05), compared with BA group the mice of ANP intervention group showed the infiltration more serious(P<0.05) in the model mice mice infiltration is more serious than the BA group, While blocking ANP signaling by A71915 mice compared with ANP mice had a significant remission(P<0.05).3.ELISA method to measure the type IFN- γ and IL- 4 levels in the BALF:compared with normal mice, the level of IL – 4 in BA mice were significantly increased, the mice of ANP group than the BA group were increased more obviously, and the levels of block the ANP signal A71915 mice compared with ANP group IL- 4 had significantly lower; compared with the normal group, BA group of IFN- γ levels in BALF reduced significantly, ANP group than BA reduce more obvious, while the mice of block the ANP signal by A71915 compared with ANP group IFN – γ level was significantly increased.4.Immunohistochemistry(IHC) technology to detect the type T – Bet and GAT A-3 protein expression level in mice lung tissue : Compared with the normal group, BA group, ANP group, the expression of GATA-3 protein increased significantly, ANP group mice increase more, and the mice of block the ANP signaling pathways by A71915 group compare with the ANP group the GATA-3protein expression was reduced;Compared to normal mice,the mice of BA group and ANP group the expression of T – Bet decreased significantly, ANP group of mice reduced more obviously, and the mice of block the ANP signaling pathways by A71915 group compare with the ANP group the T – Bet protein expression were increased significantly.5.Western blot(WB) test the expression level of NPRA 、 T-Bet and GATA-3protein in lung tissue of each groups of mice: compared with normal mice, BA,ANP group NPRA and GATA- 3 protein expression significantly increased,ANP group increased more obviously, T- bet protein expression significantly reduced, ANP group reduced more significantly(P < 0.05); the mice of block the ANP signaling pathways by A71915 group compared with ANP group,NPRA and GATA – 3 protein expression significantly reduced, T- bet protein expression is significantly increased(P < 0.05).Conclusions:1.The content of BALF and ANP in lung tissue of asthmatic mice were increased.2.ANP increased bronchial asthma airway inflammation3.ANP plays an important role in the regulation of immune balance that by the regulation of quantity and functional of type Th1/Th2 cells4.ANP signal involved in the pathogenesis of bronchial asthma...
Keywords/Search Tags:Bronchial asthma, Atrial natriuretic peptide, Transcription factor, Immune disorders
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