| Background:Acute lung injury(ALI) is a common clinical critical illness, is a combination of risk factors for pulmonary disease due to increased vascular permeability in the main clinical manifestations of pulmonary inflammation syndrome, the pathogenesis is complex and high mortality. The pathological process includes alveolar infiltration of inflam-matory cells, alveolar capillary endothelial injury, increased permeability, pulmonary edema, eventually leading to the destruction of alveolar wall integrity. There is a close correlation between lung injury in early and late reconstruction of pulmonary fibrosis. At present, there is no effective treat-ment in term of the unknown etiology and unclear pathogenesis. Endotoxin is an important factor leading to ALI. LPS induced ALI to explore the molecular mechanism of pathogenesis and new targets for intervention to reduce or prevent the occurrence and development of ALI has important clinical significance. Thus, we investigated TGF-βI receptor subtype ALK-1,2,3,5 in the normal lung tissue and the occurrence and development of ALI in the distribution and variation of selected highly expressed in ALI receptor subtype, in order to to reduce or prevent ALI.Objective:To identify the distribution and expressive changes of the subsets of TGF-βI R in normal lung and LPS-induced ALI; To explore the specific subtypes in ALI, comprehensive analysis the distribution and changes of the subsets of TGF-βI R in normal lung and ALI in the distribution and variation, for the prevention and treatment to provide a new theoretical basis for ALI.Method:We established ALI models, identified the distribution and expressive changes of the subsets of TGF-βI R in normal lung and ALI through Real Time-PCR, and selected the specific subtypes in the ALI combining with pathology.Result:1. Pathologic change by HE staining:HE staining showed both the manufacturing modules of varying degrees of alveolitis and alveolar different degrees of inflammatory cell infiltration, the most obvious in the 8h group.24h and 48h group not only showed inflammatory cell infiltration, but also seen light red liquid leaking in outside the alveolar cavity.72h group seen the phenomenon of pulmonary edema ease compared with the previous, but there is still infiltration of inflammatory cells.7th group could see reduction in the number of inflam-matory cells, edema fluid gradually absorb.2. Real Time-PCR:Compared with normal group, in the rat model of ALI established alveolar lavage TGF-βI receptor ALK-1 mRNA expression began to increase at 48h after injury and inflammation with time gradually increased, peaked at 72h, then gradually down; while the ALK-3 mRNA with the extension of lung injury with gradual increase in time, reached a peak at 24h, then decreased gradually, to 72h increased again and then decreased gradually. TGF-P I receptor subtypes ALK-5 mRNA expression increased at 8h after injection of LPS, with the injury time to extend gradually fell to its lowest level in 24h, then gradually increased, reached a peak at 7 days. ALK-2 mRNA in the low expression of injury is always in the state, did not significantly increased.Using repeated measurements analysis of variance, comparing the expressive changes between groups at different time point, we concluded that the results were P<0.05 significantly.Conclusion:ALK-1, ALK-3, ALK-5 were all highly expressed in the development of ALI and might be involved in the pathogenesis of ALI.
|
PDF Full Text Request