Forty BALB/c mice were randomly divided into 4 groups:a normal control group, an
asthma group, a vehicle control group and a
relaxin treatment group, with 10 mice in each. The mice were sensitized and challenged with
ovalbumin (OVA) to establish the chronic asthmatic model. The vehicle control group and the
relaxin treatment group were subcutaneously injected with saline and
relaxin (0.25 mg × kg(-1)× d(-1))respectively. Alteration of the airway
inflammation and
collagen deposition were observed by haematoxylin-
eosin (HE) and Masson staining.
Hydroxyproline in the lung was measured by
enzyme linked
immunosorbent assay (ELISA). The expression of α-smooth muscle actin (α-SMA) in lungs was evaluated by immunohistochemistry. The
protein expression and the
mRNA of
cyclin D(1) were detected by Western blot and RT-PCR respectively.
RESULTS: There were inflammatory cell infiltration, airway
stenosis, bronchial smooth muscle
hypertrophy and increased
collagen deposition in the asthmatic group and the vehicle control group; but these changes were significantly ameliorated in the
relaxin treatment group. The area of the α-SMA-stained smooth muscle layer in the asthmatic group and the vehicle control group was significantly greater than that in the control group (all P < 0.05), while administration of
relaxin decreased the α-SMA immunostained area (all P < 0.05). The lung
hydroxyproline content in the asthmatic and the vehicle groups [(0.68 ± 0.10) mg/g lung tissue, (0.67 ± 0.10) mg/g lung tissue] was significantly greater than that in the control group [(0.26 ± 0.05) mg/g lung tissue] (q = 16.61, 16.01 respectively, all P < 0.01). In contrast, treatment with
relaxin significantly reduced the lung
hydroxyproline content [(0.40 ± 0.06) mg/g lung tissue] compared with aforementioned 2 groups (q = 10.88, 10.26 respectively, all P < 0.05). The results of the Western blot analysis showed that the expression level of
cyclin D(1) in the asthmatic and the vehicle groups [(1.38 ± 0.18), (1.50 ± 0.10)] was higher than that in the control group (0.38 ± 0.10) (q = 13.00, 14.65 respectively, all P < 0.05), while it was significantly decreased in the
relaxin group (0.72 ± 0.13) (q = 8.51, 10.16 respectively, all P < 0.05). There were no differences in all of the parameters between the asthmatic group and the vehicle group (P > 0.05).
CONCLUSION: