Asthma is a chronic inflammatory pulmonary disease and respiratory syncytial virus (RSV) infection is a common cause of lower respiratory tract illness in infants and young children. α-Asarone presents many pharmacological effects and has been demonstrated to be useful in treating asthma. However, the functional mechanism of α-asarone in RSV-infected asthma has not been investigated. Long non-coding RNAs (lncRNAs) have been reported to play critical roles in many biological processes. Although many lncRNAs have been characterized, few were reported in asthma, especially in RSV-induced asthma. Currently, a novel post-transcriptional regulation has been proposed in which lncRNAs function as competing endogenous RNAs (ceRNAs) to competitively sponge miRNAs, thereby regulating the target genes. In the present study, we established an RSV-infected Sprague-Dawley rat model and demonstrated that lncRNA-PVT1 is involved in the mechanism of α-asarone in treating RSV-induced asthma, and lncRNA-PVT1 regulates the expression of E2F3 by functioning as a ceRNA which competitively sponges miR-203a.

No abstract

No abstract

No abstract

Asthma is considered as a difficult chronic disease with prolonged inflammation, reversible obstruction and remodeling in the airway. The present work aimed to examine the therapeutic efficacy of Bergenin-loaded Cationic Liposome (B-CLs) in asthma. We applied the thin film dispersion approach to prepare B-CLs, which were administered orally to asthma mice. Bronchoalveolar lavage fluid (BALF), cytokine contents and histopathological results were obtained and examined by transmission electron microscope (TEM), enzyme linked immunosorbent assay (ELISA) kits, together with histopathological study separately. B-CLs had a mean size of 158.33 ± 5.88 nm with positive potential of 24.51 ± 0.51 mV. In pharmacokinetics, the area under curve (AUC0–∞) and half-life (T1/2) of B-CLs were 3.33 and 3.92 times higher than free Bergenin. Compared with model group, alveolus and airway wall lesions in hematoxylin-eosin (H&E) staining of B-CLs-Medium/High dose groups declined as the wall-infiltrating inflammatory cell number declined. The thicknesses of airway wall and bronchial smooth muscle, together with the counts of bronchial smooth nuclei in B-CLs decreased significantly (P < 0.01). Specially, the ultrastructural airway changes were markedly-reversed in the B-CLs-High (P < 0.01). The changes of cytokines indicated the decrease in inflammation and improvement of the balance between T helper 1 cytokines (Th1) and T helper 2 cytokines (Th2). B-CLs could significantly enhance the dissolution, bioavailability and more inhibit airway inflammation as well as improve the lung histopathological condition.