MiR-342 attenuates lipopolysaccharide-induced acute lung injury via inhibiting MAPK1 expression.

Micro RNA (miRNA) and mitogen-activated protein kinase (MAPK) are reported as the crucial regulators of inflammatory responses in acute lung injury (ALI). This study will explore the role of the miR-342/MAPK1 axis in regulation of lipopolysaccharide (LPS)-induced ALI. We found that miR-342 was down-regulated in LPS-induced A549 cells compared with the control group with DMSO, accompanied by elevated inflammatory cytokines and apoptosis. Over-expression of miR-342 reduced LPS-induced inflammatory responses and apoptosis in LPS-stimulated A549 cells, and had a protective role in LPS-treated mice with ALI by decreasing levels of inflammatory cytokines, improving survival of mice with ALI, and ameliorating the lung permeability. Dual-luciferase reporter gene assay demonstrated that miR-342 regulated the expression of MAPK1 by directly targeting its 3' untranslated region (3'-UTR). Mechanistically, MAPK1 silencing abrogated LPS-induced inflammatory injury in A549 cells, and partially enhanced the protective effect of miR-342. Therefore, miR-342 attenuates LPS-induced ALI by targeting MAPK1 expression, thereby protecting against A549 cell injury induced by LPS and lung injury of mice with ALI.

Effect of physiological pH on the molecular characteristics, rheological behavior, and molecular dynamics of κ-carrageenan/casein.

Introduction: During gastrointestinal digestion, κ-carrageenan (κ-CGN) undergoes physicochemical changes, which associated with the risk of colitis. Methods: To understand the effect of physiological pH on the conformational transition and binding stability of κ-CGN and κ-carrageenan/casein (κ-CC), we conducted experiments at pH 3.0 (gastric environment) and pH 7.0 (intestinal environment). We evaluated zeta potential, free sulfate group content, Fourier transform infrared spectroscopy, thermodynamic properties, microstructure, and molecular mechanism. Results and Discussion: Our results revealed that the helical conformation of κ-CGN and κ-CC were more ordered and stable, and sulfate group exposure both lower in the intestinal environment (pH 7.0). However, in gastric environment (pH 3.0), the charge density of κ-CGN decreased, accompanied by random curling conformation and free sulfate group content increased. In contrast, the intermolecular interactions between κ-CGN and casein increased in gastric acid environments due to casein flocculation and secondary structure folding, and significantly reduced the exposure of free sulfate groups of κ-CGN. Our research results provide an important theoretical basis for elucidating the molecular mechanism and structure-activity relationship of κ-CGN under casein matrix to protect the mucosal barrier and inhibit colitis, and are of great significance for guiding and expanding the safe application of κ-CGN, thus assisting food nutrition to be absorbed.

Ultrasound-assisted solubilization of calcium from micrometer-scale ground fish bone particles.

In order to promote the extraction of biological calcium from fish bone, ultrasonication was used to process micrometer-scale fish bone particles (MFPs) and investigate the mechanism of action in relation to bone structure. With ultrasonication treatment (300 W, 60°C, 2 h), the content of calcium release increased by 25.6%. Calcium release reached 94.0% of total calcium after 24-h treatment. The surface of the MFPs was significantly damaged by ultrasound-induced cavitation, resulting in holes and separation of the layered structure. X-ray diffraction (XRD) and Fourier transform infrared (FT-IR) analysis demonstrated that the crystalline structure of hydroxyapatite was disrupted, the triple helical structure of mineralized collagen fibrils (MCFs) was loosened, and hydrogen bonding in collagen decreased, facilitating the release of hydroxyapatite crystals. Thus, ultrasonication may be a practical alternative to nanomilling for industrial processing of waste fish bones to produce soluble calcium as an ingredient in calcium supplements and supplemented foods.

MiR-216a alleviates LPS-induced acute lung injury via regulating JAK2/STAT3 and NF-κB signaling.

MicroRNAs (miRNAs) play an important role in the progression of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Till now, little is known about the role of miR-216a in ALI/ARDS. In this study, patients with ARDS exhibited significantly higher interleukin-1ß (IL-1ß), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels than healthy controls (P < 0.01). However, miR-216a expression in patients with ARDS was significantly lower than healthy controls (P < 0.05), and negatively correlated with 28-day survival rate. Similar effects were observed in LPS-treated mice and A549 cells. MiR-216a over-expression reduced LPS-induced IL-1ß, IL-6 and TNF-α levels, and ameliorated lung permeability, and prolonged overall survival of ALI mice. Further, miR-216a over-expression inhibited LPS-induced apoptosis and autophagy. In addition, the janus kinase-2 (JAK2) was a direct target of miR-216a. Silencing of JAK2 partially aggravated miR-216a-inhibited inflammation injury. Besides, miR-216a obviously decreased the expressions of phosphorylated signal transducer and the activator of transcription 3 (p-STAT3), p-p56, and p-IκBα. In conclusion, miR-216a alleviates LPS-induced inflammatory injury via regulating JAK2/STAT3 and NF-κB signaling.