Objective To explore the effect of Shugan Lifei prescription on expression of Transforming Growth Factor-beta1(TGF-β1) and Smad3 in asthma rats under chronic stress condition. Method The 40 SD rats were randomly divided into four groups:control group, model group, dexamethasone group and Shugan Lifei group. Asthma model was established by inhaling atomized ovalbumin (OVA) passively and experiencing chronic unpredictable mild stress (CUMS). From the 15th day of modeling, the treatment groups were intervened with dexamethasone drugs and Shugan Lifei prescription. Lung pathomorphology was observed via HE staining. The expressions of TGF-β1 and Smad3 in lung tissue were measured by immunohistochemical and RT-PCR. Results Compared with control group, the wall area and the smooth muscle area in the model group significantly increased. While compared with asthmatic model group,the wall area and the smooth muscle area in the dexamethasone group and Shugan Lifei group were significantly lower. Immunohistochemistry and RT-PCR showed that in comparison with control group , the expression of TGF-β1/Smad3 protein and mRNA in lung tissues in the model group significantly increased(P<0.05), while the TGF-β1/Smad3 protein and mRNA in lung tissues in the dexamethasone group and Shugan Lifei group were detected to be significantly lower than model group (P<0.05). Conclusion Shugan Lifei method could improve airway remodeling in asthma rats under chronic stress condition , and this result is possibly achieved by reducing TGF-β1 and Smad3 expression levels.

BACKGROUND:Poly(butylene succinate) (PBS) and polypropylenecarbonate (PPC) are new medical materials developed in recent years, characterized as good biocompatibility, biodegradability and the low price. OBJECTIVE:To prepare the PBS/PPC biofilm by electrostatic spinning method and evaluate its physical and chemical properties, degradation performance and effect on cel proliferationin vitro. METHODS:The PBS/PPC biofilm was prepared using electrostatic spinning method: 0.9 g PBS and 0.9 g PPC were dissolved in 10 mL of trichloromethane at room temperature and stirred magneticaly until they were fulydissolved. Then, the spinning solution was added into a spinning tube with a distance of about 15 cm and at a voltage of 18 kV. The surface morphology was observed by scanning electron microscopy. The intensity, contact angle and water absorption, pH value and weight loss in the process ofin vitro degradation were measured. MG63 cels were co-cultured with the biofilm for 7 days and cel proliferation was detected by cel counting kit-8. RESULTS AND CONCLUSION: The PBS/PPC biofilm showed a porous structure with interconnected pores. The fiber diameter was about 0.88 μm, the average aperture was about 5.68 μm, the porosity was 78.3%, the fracture intensity was 2.31 MPa, the elongation rate at break was 23.48%, the average value of contact angle was 87°, and the water absorption rate was 68.54%. During the biofilm degradation, the pH value decreased gradualy andreduced to 6.76 at 12 weeks; meanwhile, the biofilm degraded equaly and gradualy, and the weight loss rate was 6.04% at the end of the 12th week. The results of cel counting kit-8 showed that the PBS/PPC biofilm could promote cel proliferation. Overal, the PBS/PPC biofilm has good physical and chemical properties, good space-making feature, wettability and degradability, which can provide sufficient time for bone tissue regeneration.

There are different degrees of bone defect in immediate implantation for anterior dentition. During conventional guided bone regeneration, the wound was difficultly closed in operation,and there was more inflammatory response and infection risk. In this paper,a case of immediate implantation for anterior dentition combined with platelet rich-fibrin(PRF) was reported,the clinical effects of guiding bone regeneration and alleviating the inflammatory response.

Objective To investigate the long non-coding RNA(lncRNA) MRAK08838 regulates macrophage function to influence the development of asthmatic airway inflammation. Methods MRAK088388 gene knockout (MRAK088388^-/-) mouse model was prepared and allergic asthma was induced by dust mite protein Dermatophagoides farinae 1 (Der f1). The mice were sacrificed after 28 days of modeling, and serum was collected to measure IgE and IgG. The FinePointe RC system was used to measure airway hyperresponsiveness and evaluate lung function in mice. Lung tissue was taken for HE staining, and periodic acid-Schiff (PAS) staining was used to evaluate inflammatory infiltration and mucus secretion in mouse lungs. Fluorescence quantitative PCR was used to detect the expression level of lncRNA MRAK08838 in bronchoalveolar lavage fluid (BALF) cells and lung tissue of asthmatic mice. ELISA was used to detect the levels of inflammatory cytokines IFN-γ, IL-4, IL-5, IL-13, IL-10 and IL-17A. Flow cytometry was used to evaluate the phenotype of macrophages in BALF and lung tissue, as well as the proportion of neutrophils, eosinophils, and alveolar macrophages. The changes of the above indicators were detected in mice by adoptive transfer of bone marrow-derived macrophages (BMDM). Results Under the challengle of Der f1, MRAK088388^-/- mice showed reduced allergic airway inflammation, including reduced eosinophils in BALF and reduced production of IgE and IgG1. In addition, Der f1-treated MRAK088388^-/- mice had fewer M2 macrophages than wild-type asthmatic mice. Wild-type mouse BMDM (M0) and Der f1-treated MRAK088388^-/- mice also showed mild inflammatory response. Conclusion Knockout of MRAK088388 alleviates airway inflammation in asthmatic mice by inhibiting M2 polarization of airway macrophages.
Animals ; Mice ; Mice, Knockout ; RNA, Long Noncoding/genetics* ; Asthma/genetics* ; Macrophages ; Immunoglobulin E

【Objective】 To investigate the association between the long-stranded non-coding ribonucleic acid (lncRNA) MRAK088388 and allergic asthma in children. 【Methods】 A total of 15 healthy children and 15 children with asthma were monitored for disease progression over a 2-year period. Blood samples were collected from patients during the chronic phase of the disease for lncRNA/mRNA expression microarray analysis. Competing endogenous RNA networks (MRAK088388/miR-30a/ATG5) were identified by bioinformatics analysis. In vitro cultured bronchial epithelial (16HBE) cells were used to quantify gene and associated protein expression levels by real-time fluorescent quantitative polymerase chain reaction (qPCR) and protein blotting, respectively. Cell Counting Kit-8 and transwell assays were used to assess the proliferation and migration of 16HBE cells and verify the effects of MRAK088388, miR-30a and ATG5 on asthma. 【Results】 Six lncRNA-miRNA-mRNAs were identified by correlation analysis. By qRT-PCR analysis, MRAK088388/miR-30a/ATG5 was selected to construct the ceRNA network in this study. mRAK088388 and ATG5 expressions were high in the peripheral blood of children with asthma, while the expression of miR-30a was low (P<0.05). The expression level of E-cadherin was significantly higher in 16HBE cells after si-MRAK088388+TGF-β1 group, while the expression levels of Vimentin and α-SMA were significantly lower (P<0.05), indicating that knockdown of MRAK088388 inhibited the epithelial mesenchymal transition in 16HBE cells. Compared with si-NC+ TGF-β1 group, the cell morphology of si-MRAK088388+TGF-β1 group was similar to that of the control group, indicating that MRAK088388 knockdown attenuated TGF-β1-induced cell morphological changes; in addition, MRAK088388 knockdown inhibited TGF-β1-induced proliferation and migration of 16HBE cells. MRAK088388 was confirmed by qPCR and protein blotting to promote the progression of childhood asthma by targeting the miR-30a/ATG5 axis. 【Conclusion】 Childhood asthma is associated with the MRAK088388/miR-30a/ATG5 axis, and MRAK088388 is involved in the process of childhood allergic asthma by negatively regulating miR-30a expression and regulating elevated ATG5 expression levels to affect bronchial epithelial cell mesenchymal transition, proliferation, and migration.