Combination of TLR agonist and miR146a mimics attenuates ovalbumin-induced asthma.

BACKGROUND: microRNA-146a has been reported to be a regulator in the process of attenuating asthma by inhibiting Toll-like receptor 2 (TLR2) pathway. This study aimed to investigate how miR146a-inhibitor affect the symptom of asthma and the underlying mechanisms. METHODS: Ovalbumin (OVA)-induced allergic asthma mice model was established by intraperitoneal injection with 20 µg of OVA. Total cells and differential inflammatory cells in bronchoalveolar lavage fluid were counted by flow cytometry. The expression levels of molecules and cytokines in TLR2 signaling pathway were detected by Q-PCR and ELISA. RESULTS: miR146a-inhibitor attenuated OVA-induced allergic asthma by increasing Th1 cytokines in OVA-induced allergic asthma model, and the treatment of miR146a-inhibitor can reduce the inflammation caused by asthma, followed by the down-regulation of IL-5 and IL-13 in sorted ILC2. The inhibition of miR-146a significantly reduced symptoms of asthma model with TLR2-related molecules being up-regulated. CONCLUSION: It was found that miR-146a is an important regulator in OVA-induced allergic asthma model, which can relieve symptoms of asthma through regulating TLR2 pathway. These findings provide a theoretical basis for solving asthma in clinical treatment.

Rosiglitazone Reduces Apoptosis and Inflammation in Lipopolysaccharide-Induced Human Umbilical Vein Endothelial Cells.

BACKGROUND Although the peroxisome proliferator-activated receptor-g (PPARg) agonist rosiglitazone has significant anti-inflammatory properties, no scientific studies have provided new insights in its pharmacological properties with respect to acute respiratory distress syndrome (ARDS). The present investigation aimed to evaluate whether rosiglitazone can reduce apoptosis and inflammation in a lipopolysaccharide (LPS)-induced acute respiratory distress syndrome in vitro model. MATERIAL AND METHODS Human umbilical vein endothelial cells (HUVECs) were treated with 1 µg/ml LPS in the absence or presence of 10 µM rosiglitazone for 24 h. Cell viability was measured by MTT assay. Flow cytometry was used to examine the cell apoptosis and ROS production in HUVECs response to LPS and rosiglitazone. The levels of pro-inflammatory cytokine factors, including TNF-α, IL-6, CXCL12, and CXCR4, were measured by ELISA, real-time PCR, and Western blot assay, respectively. The expression of PPARg, Bcl-2, and Bax and the activity of JAK2 and STAT3 were also investigated by Western blot assay. RESULTS We found that rosiglitazone significantly inhibited LPS-induced cell apoptosis, ROS production, and inflammation in HUVECs. Furthermore, we found a significant reduction of JAK2/STAT3 activation and the Bax/Bcl-2 ratio in LPS-induced HUVECs response to rosiglitazone treatment. CONCLUSIONS Treatment with rosiglitazone can reduce apoptosis and inflammation in HUVECs induced by LPS.

Cyclic Polyesters with Closed-Loop Recyclability from A New Chemically Reversible Alternating Copolymerization.

Polyesters with both cyclic topology and chemical recyclability are attractive. Here, the alternating copolymerization of cyclic anhydride and o-phthalaldehyde to synthesize a series of cyclic and recyclable polyesters are reported for the first time. Besides readily available monomers, the copolymerization is carried out at 25 °C, uses common Lewis/Brønsted acids as catalysts, and achieves high yields within 1 h. The resulting polyesters possess well-defined alternating sequences, high-purity cyclic topology, and tunable structures using distinct two monomer sets. Of interest, the copolymerization manifests obvious chemical reversibility as revealed by kinetic and thermodynamic studies, making the unprecedented polyesters easy to recycle to their distinct two monomers in a closed loop at high temperatures. This work furnishes a facile and efficient method to synthesize cyclic polyesters with closed-loop recyclability.