Bioavailable and less toxic synthetic retinoids, such as the atypical adamantyl retinoid ST1926, have been well developed and investigated in clinical trials for many diseases. The aim of our study was to explore the role of ST1926 in lipopolysaccharide (LPS)-induced acute lung injury (ALI) and to reveal the possible molecular mechanism. Mice were treated with LPS to induce acute lung injury followed by ST1926 administration. After LPS induction, mice administered with ST1926 showed lower inflammation infiltration in bronchoalveolar lavage (BAL) fluid, and pro-inflammatory cytokines, including interleukin-1β (IL-1β), IL-18, IL-6 and tumor necrosis factor-α (TNF-α) in serum and lung tissue samples obtained from mice. In addition, western blot assays suggested that ST1926 suppressed nuclear factor-κB (NF-κB), inhibitor-κB kinase-α (IκBα) and IκB kinase (IKKα), as well as Toll-like receptor 4 (TLR4) induced by LPS. In addition, reactive oxygen species (ROS) stimulated by LPS was also suppressed for ST1926 through inhibiting p38 and extracellular receptor kinase (ERK) signaling pathway. Taken together, the data here indicated that ST1926 may be of potential value in treating acute lung injury through inflammation and ROS suppression via inactivating TLR4/NF-κB and p38/ERK1/2 signaling pathways.

Acute lung injury in children is a complication showing devastating disorders linked to fibrosis progression and inflammation response. Fibrosis and inflammation response are two markers for acute lung injury. Juglanin is a natural product mainly isolated from green walnut husks of Juglans mandshurica, which isconsidered as the functional composition among a series of compounds. It exhibited effective role in various diseases by inhibiting inflammation response. In our study, the protective effects and anti-inflammatory activity of juglanin were investigated in mice and lung cells treated by lipopolysaccharide (LPS) to reveal the possible mechanism by which juglanin attenuates acute lung injury. The mice were separated into four groups. The mouse model was established with 15 mg/kg LPS injection. Juglanin dramatically reduced the inflammation of cell infiltration. Compared to mice only treated with LPS, LPS-treated mice in the presence of juglanin developed less lung fibrosis with lower levels of α-smooth muscle-actin (α-SMA), collagen type I, collagen type III, and transforming growth factor-β1 (TGF-β1). Additionally, juglanin markedly downregulated inflammatory cytokine secretion and phosphorylated nuclear factor-κB (NF-κB) expression via inhibiting IKKα/IκBα signaling pathway. Our results indicate that juglanin has a protective role in LPS-triggered acute lung injury via suppression of fibrosis and inflammation response by NF-κB signaling pathways inactivation. Thus, juglanin may be a potential candidate as dietary supplement for acute lung injury for children in future.

The aim of the study was to investigate the antiasthmatic effects of eugenol (EUG) and the possible mechanisms. Asthma model was established by ovalbumin induction. A total of 50 mice were randomly assigned to five experimental groups: control, OVA, OVA + dexamethasone (2 mg/kg), OVA + EUG (10 mg/kg), and OVA + EUG (20 mg/kg). Airway resistance (Raw) were measured, histological studies were evaluated by the hematoxylin and eosin (HE) staining, interleukin-4 (IL-4) and interleukin-5 (IL-5) were evaluated by enzyme-linked immunosorbent assay (ELISA), Vitamin D3 upregulated protein 1 (VDUP1), IκBα, P-IκBα, NF-κBP65, and p-NF-κBP65 were measured by Western blotting. Our study demonstrated that EUG inhibited OVA-induced increases in Raw and eosinophil count; IL-4 and IL-5 were recovered. Histological studies demonstrated that EUG substantially inhibited OVA-induced eosinophilia in the lung tissue. Western blotting studies demonstrated that EUG substantially inhibited P-IκBα, NF-κBP65, and p-NF-κBP65 protein levels and increased VDUP1 and IκBα protein levels. These findings suggest that EUG may effectively ameliorate the progression of asthma and could be used as a therapy for patients with allergic asthma.