Abstract:
Introduction: Bronchial asthma (BA) is a serious problem in all countries irrespective of the level
of their development. Prevalence of the disease fluctuates, depending on the region, and averages in the
majority of the states from 2 to 25,5 %. Annually, all over the world, BA carries away about 250 thousand
lives, many of which could be saved with adequate treatment and educating the patients. In present, there
is a rise of illness growth with BA and actual experimental modeling of the given disease for the purpose
of a fuller understanding of pathogenesis and working out ethiopathogenetical therapy methods. In the
literature, a variety of experimental models BA with animals which are used for studying various aspects
of pathogenesis and approbations of new ways of treatment is described. At the same time each model
has certain features which limit the sphere of its use. For today, the urgency of such works is increased
in connection with the detection of new markers of BA and, accordingly, new directions of pathogenesis
BA research and to search for pathogenetical well-founded methods of treatment. We first hypothesized
that the reduced sensitivity to corticosteroids in bronchial asthma may be due to increased expression of
P-glycoprotein (Pgp).
Objective: To study the nature of the coupling CD38-and Pgp-dependent mechanisms of hypereactivity and bronchial steroid-sensitive allergic animals to create a concept to overcome the reduced sensitivity to corticosteroids in bronchial asthma. Materials and methods: The objects of research are laboratory animals (rats) of both sexes at the
age of 6-7 weeks. Group 1 - rats with simulated asthma; group 2 - animals with a simulated asthma and
“treated” glucocorticosteroid (GCS), dexamethasone; group 3 - the control group (nonallergic);
Results: In the process, an experimental simulation of asthma in animals, assessment of clinical
signs allergization ovalbumin, and immunocytochemical study of preparations of bodies of animals and
spectrofluorimetrical research of preparations of animal bodies were carried out. The study obtained
a model of bronchial asthma in rats, confirmed clinically, and found that: the expression of CD38 was
higher in group 1 rats; the activity of CD38 in experimental models of asthma is the highest at the site of
localization of the inflammatory process, i.e. in the lungs; revealed a positive correlation relationship (r
= 0,720894) between the activity of ADP-ribozilciklazy in the tissues of lung and spleen in the first group
of animals suggests that the activity of CD38 is increased in asthma, not only in the lungs, but also in the
spleen; the level of Pgp expression did not differ in rats with simulated asthma and control groups.
Conclusions: It would be desirable to notice that now already there are modulators of activity in both
expression of Pgp and CD38 which demand the further studying and in the future could be used for
treatment BA.
