Expression Of IL-21,MMP-9and TIMP-1in Mice With Asthma And The Effect OF Budesonide On The Expression

Objective:To study the expressions of Interleukin21(IL-21), matrix metalloproteinase-2(MMP-2) and tissue inhibitor of matrix metallo-proteinases-1(TIMP-1) in lung tissue of asthma mice; To observe whether IL-21will affect the secretion of MMP-2and change the balance between MMP-2and TIMP-1so as to participate in the airway remodeling of asthma mice; To observe whether the inhaled glucocorticoid, budesonide, will affect the IL-21level in lung tissue of asthma mice.Methods:Mice model of asthma was created with ovalbumin (OVA) sensitization and activation. BALB/c female mice were selected as the experimental animals. The36mice were randomly divided into3groups, with12in each group. The first group was the normal saline control group (CTRL group), the second group was OVA sensitization and activation of asthma group (OVA group) and the third group was the budesonide intervention group (OVA+BUD group). Observe the lung tissue in each group of mice for HE staining and Masson staining, to determine whether the mice model of asthma was successfully established; Conduct immunohistochemical detection for the expressions of MMP-2and TIMP-1protein in the airway and lung tissue in each group of mice; Conduct RT-PCR detection for the expressions of IL-21mRNA in the small airway and lung tissue in each group of mice.Results:1.HE staining of lung tissue paraffin section shows:the small airway epithelial cells in OVA group of mice have fallen off, with the necrosis, structure disorder and proliferation of goblet cells, The small airway duplicature is increased and thickened, with the infiltration of peribronchial and perivascular inflammatory cells; The alveolar septum becomes wider and the alveolar wall becomes thinner or even fractured; The HE staining airway epithelial cells in CTRL group of mice are normal, without the infiltration of peribronchial and perivascular inflammatory cells, and the alveolar walls are intact; The above performance in OVA+BUD group of mice is significantly lower than that of OVA group.Masson staining shows:a lot of collagen fiber deposition is visible around the small airway and blood vessels in OVA group of mice; The Masson staining in CTRL group of mice are normal, without visible collagen fiber deposition around small airway, only with a little collagen fiber deposition around the blood vessels; The above performance in OVA+BUD group of mice is significantly lower than that of OVA group.The above results show the asthma mice model has been successfully established.2.The expressions of MMP-2and TIMP-1protein in the three groups of mice airway and lung tissue:the expressions of MMP-2and TIMP-1as well as MMP-2/TIMP-1ratio in OVA group are higher than those of CTRL group and CTRL+BUD group, where the difference is statistically significant (P<0.05); To compare the expressions of MMP-2and TIMP-1as well as MMP-2/TIMP-1ratio in both the CTRL group and OVA+BUD group, the difference is not significant (P>0.05).3. The expressions of IL-21mRNA in three groups of airway and lung tissue:the expression level of IL-21mRNA in the small airway and lung tissue in OVA group of mice is lower than that of CTRL group and OVA+BUD group, where the difference is statistically significant (P <0.05); the expression level of IL-21mRNA in the small airway and lung tissue in CTRL group is higher than that of OVA+BUD group, the difference is statistically significant (P<0.05).Conclusions:1.The expression of IL-21in the lung tissue of asthma mice is lower than that of mice in normal saline control group and budesonide intervention group;The expression of MMP-2and TIMP-1and MMP-2/TIMP-1ratio in the lung tissue of asthma mice are higher than those of CTRL group and CTRL+BUD group.2. After the intervention of budesonide, the expression of IL-21in the lung tissue of asthma mice is up-regulated, and the expression of MMP-2and TIMP-1and MMP-2/TIMP-1ratio is down-regulated.3. Both the expressions of IL-21and MMP-2and TIMP-1and MMP-2/TIMP-1ratio in the lung tissue of asthma mice are negatively correlated.