The Change Of Osteopontin Expression In Bronchial Lung Tissue Of Asthma Rat Model And Its Probably Regulatory Mechanism

Objective To investigate the expression of osteopontin(OPN) in bronchial lung tissue of asthma rat model and the influence of dexamethasone on OPN expression in bronchial lung tissue of asthma rat model. To reveal the roles of OPN in the pathophysiologic process of asthma and the possible regulatory mechanisms. Methods Twenty-four SD rats were randomly divided into control group (group A), asthma model group (group B), DXM group (group C), 8 rats each group. Asthma rat model was established by sensitization and stimulation with ovalbumin(OVA) together with immune adjuvant aluminium hydroxide. Bronchial lung tissue slices were stained with HE to observe the morphologic changes of bronchial lung tissue. The expression of OPN in bronchial lung tissue of the rats of three groups was detected by immunohistochemistry to analyse its role in asthma . OPN expression and phosphorylation levels of ERK, p38 in bronchial lung tissue of the rats of three groups were analysed by Western Blot to reveal the regulation of OPN expression and the possilbe mechanism of DXM in asthmatic attack management. Results HE staining showed that there was bronchial contraction and bronchiolar epithelium partially desquamated in the asthma model group rats. And lots of inflammatory cell infiltration such as eosinophils and neutrophils arround bronchial was observed in in the asthma model group rats but just a few of these cells were detected in DXM group rats. There is no apparent abnormality in control group rats. The results of immunohistochemistry showed that the expression of OPN in bronchial lung tissue of asthma model group and DXM group rats was markedly increased compared with control group(P<0.05). And OPN expression in DXM group was significantly less than asthma model group. The results of Western blot confirmed that the expression of OPN in bronchial lung tissue of asthma model group was markedly increased compared with control group(P<0.05) and there is a dramatically diminished OPN expression in DXM group. This is consistent with the immunohistochemistry results. Western blot also showed that the phosphorylation level of ERK in bronchial lung tissue of asthma model group was significantly increased than that in control group and it was greatly reduced in DXM group compared to asthma model group(P<0.05). The phosphorylation levels of p38 had no difference between asthma model group and control group, but was obviously decreased in DXM group compared to control group and asthma model group. Conlusion OPN expression and the phosphorylation level of ERK in bronchial lung tissue is significantly increased in bronchial lung tissue of asthma group. This suggests that OPN plays a role in asthma and its expression is up-regulated by ERK/MAPK signal pathway. OPN expression and the phosphorylation level of ERK and p38 are all obviously diminished in DXM group. This suggests that DXM may inhibit both ERK/MAPK and p38/MAPK signal pathway to decrease the expression of OPN. Therefore, we consider that OPN inhibition is Part of the reason why glucocorticoid coulld effectively treat the asthma.