| Background: Bronchial asthma is a kind of chronic airway inflammation, in which eosinophils, mast cells and T lymphocytes are involved. Eosinophils infiltration and bronchial hyperreactivity are characteristic features of asthma. Infiltration and activation of eosinophils is important for asthma pathogenesis. It is known that in airway inflammation of asthma, many factors take part in eosinophils chemotaxis, infiltration, and activation, and the release of inflammatory mediators. Recently, it is considered that adhesion molecules, especial vascular adhesion molecule-l(VCAM-J)/ very late antigen-4(VLA-4), are very important for the eosinophils to be adhered to vascular endothelia, trans endothelia and at last infiltrated in the lung tissue. In our experiments using rat bronchial asthma model, we found that the expression of VCAM-1 was enhanced directly after ovalbumin (OVA) sensitization, and the enhancedexpression was not increased further by OVA challenge. We also found that the down regulation effect on the enhanced VACM-I is one of the anti-asthmatic mechanisms of dexamethasone,but not that of SR I4033,a selective NK-I receptor antagonist . So it was thought that VCAM-1 up-regulation is a phenomenon occurred after sensitization.AIM: This study aims to confirm the expression and pharmacological modulation of vascular cell adhesion molecule-1 (VCAM-1) after OVA sensitization and challenge in the isolated lung slices, with emphasis on the possible effects of dexamethasone, a classical anti-asthmatic drug, ONO-1078,{4-oxo-8-[p-(4-phenylbutyloxy)benzoyl-amino ]-2-( tetrazol-5-l )-4 //-1-benzopyran hemihydrate }, a potent leukotriene receptor antagonist, SR 140333, a selective NK-1 receptor antagonist.METHODS: rats were killed 15 days after ovalbumin(lmg/ml) sensition and the lungs were removed and cut into lung slices about 500 u m thickness. The lung slices were incubated in the Kreb's solution which was saturated with mixed gas ( 95%O2 and 5%CO2) at temprature 35盜癈. After Ih of incubation the lung slices were added with drugs or saline (as controls), OVA or saline was given lOmin late, the lung slices was removed after another 3h incubation and stored at -70癈. To determine the viability of the lung slices in the Kreb's solution we assessed the LDH (lactate dehydrogenase) release from the slices. At last the protein expression of VCAM-1 in the lung slices was determined by westernblotting.RESULTS:1. LDH was released from the lung slices during incubation in conditioned Kreb's solution. In the first Ih the release of LDH was high and not stable, but the release was lower and stable in the following 3h, OVA challenge did not change the release.2. The effects of OVA-sensitization and OVA challenge on the VCAM-1 expression of lung slices. VCAM-1 was expressed in the lung slices from non-sensitized rats without OVA challenge in vitro (n=8, 1.08 ?0.14). There was no significant difference between the expression of VCAM-1 in lung slices challenged in vitro with OVA (n=8, 1.06 ?0.20) and with saline from non-sensitized rats. But the expression of VCAM-1 in lung slices from OVA-sensitized rats challenged with saline in vitro (n=8, 1.38 ?0.21) were much more ( about 28% increment ) than in lung slices from non-sensitized rats challenged with saline in vitro. But there was no more statistical increment in VCAM-1 expression of lung slices challenged with OVA in vitro (n=8, 1.54 ?0.31) than challenged with saline in vitro, all of them were gotten from sensitized rats.3. The effect of drugs on VCAM-1 expression of lung slices from non-sensitized rats .a. Treated with dexamethasone at concentration of 0.1 u mol/L , the VCAM-lexpression of the slices [no challenged: n=8, 0.88 ?0.25(relative expression); challenged with OVA: n=8, 0.93 ?0.13(relative expression)]were a little less than the controls with no statistical significance. But treated with dexamethasone at concentration of l.Ou mol/L the VCAM-lexpression of the slices [no challenged: n=8, 0.73...
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