Title: EFFECTS OF LAMINARIN ON AIRWAY INFLAMMATION AND EXPRESSIONS OF IL-12,IL-13 AND TGF-Β1 IN BRONCHOALVEOLAR LAVAGE FLUID OF ASTHMATIC MICE
Abstract: Objective To explore the effects of laminarin on airway inflammation,expressions of interleukin-12(IL-12),interleukin-12(IL-13)and transforming growth factor beta 1(TGF-β1)in bronchoalveolar lavage fluid(BALF)of asthmatic mice.Methods Forty SPF mice were equally randomized to four groups:asthma model group,budesonide group,laminarin group,and control group.In the model group,an asthmatic rat model was created by intraperitoneal injection of ovoalbumin(OVA)and aerosol inhalation OVA motivating for two weeks;in laminarin group and budesonide group,the rats in each group were offered laminarin(50mg/kg)intragastric administration and budesonide(200μg)inhalation,repectively.The histological changes in the bronchi and alveoli in each group were observed under microscope by HE staining and the expression levels of IL-12,IL-13,and TGF-β1in BALF were detected by enzyme linked immunosorbent assay(ELISA). Results After two-week allergen excitation,more typical asthma-like changes appeared in lung tissues of rats in the model group,the changes in the laminarin group and budesonide group decreased.Compared with the control group,the levels of IL-12in BALF in the model group declined,and that of IL-13and TGF-β1elevated(F=18.01-52.51,q=9.93-17.12,P0.05).Compared with the model group,the levels of IL-12in rats in laminarin group and budesonide group elevated,and IL-13and TGF-β1declined,but still higher than the normal control group(q=2.91-12.59,P0.05).A comparison between laminarin group and budesonide showed the differences of each cytokine were significant(q=3.06-3.54,P0.05). Conclusion Laminarin can inhibit the expressions of IL-13and TGF-β1,raise the expression of IL-12in BALF of asthmatic rats to a certain extent and antagonise inflammation of respiratory tract,thus provides a new approach for the therapy of asthma.
Publication Year: 2014
Publication Date: 2014-01-01
Language: en
Type: article
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