Effects of microplastics on microbial community structure and wheatgrass traits in Pb-contaminated riparian sediments under flood-drainage-planting conditions.

The coexistence of microplastics (MPs) and heavy metals in sediments has caused a potential threat to sediment biota. However, differences in the effects of MPs and heavy metals on microbes and plants in sediments under different sediment conditions remain unclear. Hence, we investigated the influence of polyethylene (PE) and polylactic acid (PLA) MPs on microbial community structure, Pb bioavailability, and wheatgrass traits under sequential incubation of sediments (i.e., flood, drainage, and planting stages). Results showed that the sediment enzyme activities presented a dose-dependent effect of MPs. Besides, 10 % PLA MPs significantly increased the F1 fractions in three stages by 11.13 %, 30.10 %, and 17.26 %, respectively, thus resulting in higher Pb mobility and biotoxicity. MPs altered sediment bacterial composition and structures, and bacterial community differences were evident in different incubation stages. Moreover, the co-exposure of PLA MPs and Pb significantly decreased the shoot length and total biomass of wheatgrass and correspondingly activated the antioxidant enzyme activity. Further correlation analysis demonstrated that community structure induced by MPs was mainly driven by sediment enzyme activity. This study contributes to elucidating the combined effects of MPs and heavy metals on sediment ecosystems under different sediment conditions.

The role of novel adipokines and adipose-derived extracellular vesicles (ADEVs): Connections and interactions in liver diseases.

Adipose tissues (AT) are an important endocrine organ that secretes various functional adipokines, peptides, non-coding RNAs, and acts on AT themselves or other distant tissues or organs through autocrine, paracrine, or endocrine manners. An accumulating body of evidence has suggested that many adipokines play an important role in liver metabolism. Besides the traditional adipokines such as adiponectin and leptin, many novel adipokines have recently been identified to have regulatory effects on the liver. Additionally, AT can produce extracellular vesicles (EVs) that act on peripheral tissues. However, under pathological conditions, such as obesity and diabetes, dysregulation of adipokines is associated with functional changes in AT, which may cause liver diseases. In this review, we focus on the newly discovered adipokines and EVs secreted by AT and highlight their actions on the liver under the context of obesity, nonalcoholic fatty liver diseases (NAFLD), and some other liver diseases. Clarifying the action of adipokines and adipose tissue-derived EVs on the liver would help to identify novel therapeutic targets or biomarkers for metabolic diseases.

Core fucosylation regulates alveolar epithelial cells senescence through activating of transforming growth factor-ß pathway in pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF), a fatal disorder associated with aging, has a terrible prognosis. However, the potential causes of IPF remain a riddle. In this study, we designed to explore whether the modification of the core fucosylation (CF) can ameliorate pulmonary fibrosis by targeting alveolar epithelial cells (AECs) senescence. First, we verified that cellular senescence occurs in the bleomycin-induced lung fibrosis mice models and CF modifications accompanying senescent AECs in pulmonary fibrosis. Next, both gain- and loss- of function research on CF were performed to elucidate its role in promoting AECs senescence and triggering pulmonary fibrosis in vitro. Notably, using alveolar epithelial cell-specific FUT8 conditional knockout mouse models, however, inhibition of cellular senescence by deleting the FUT8 gene could attenuate pulmonary fibrosis in vivo. Finally, blocking the CF modification of transforming growth factor -ß type I receptor (TGF-ßR I) could reduce the activation of downstream transforming growth factor -ß (TGF-ß) pathways in AECs senescence both in vivo and in vitro. This study reveals that CF is a crucial interventional target for the treatment of pulmonary fibrosis. Blocking CF modification contributes importantly to inhibiting AECs senescence resulting in pulmonary fibrosis lessen.

Structural characterisation and antioxidant activities in vitro and in vivo of a novel polysaccharide from Salvia miltiorrhiza.

Polysaccharides have received extensive attention due to their multiple physiological functions, especially their remarkable antioxidant capacity. In this study, a novel acidic polysaccharide (PSMP-2) with a molecular weight (Mw) of 1.28 × 106 Da from Salvia miltiorrhiza Bunge was extracted and purified via DEAE-52 cellulose column and Sephadex G-100 column chromatography. The structure of PSMP-2 was characterised by high-performance gel permeation chromatography (HPGPC), high-performance liquid chromatography (HPLC), Fourier transforms infrared spectroscopy (FT-IR) and methylation analysis. The results showed that PSMP-2 was an acidic heteropolysaccharide composed of rhamnose (Rha) (6.15%), galacturonic acid (GalA) (55.98%), and galactose (Gal) (21.27%) and arabinose (Ara) (16.69%). PSMP-2 contained five major glycosidic linkages, (1→)-linked-Ara, (1→2, 4)-linked-Rha, (1→4)-linked-Gal, (1→6)-linked-Gal, (1→3, 6)-linked-Gal, in a molar ratio of 5.98: 1.45: 72.23: 16.40: 3.94. The IC50 of PSMP-2 on 2, 2-Diphenyl-1-picrylhydrazyl (DPPH) and hydroxyl free radical scavenging ability were 0.991 mg/mL and 4.007 mg/mL, respectively. It could regulate the activity of antioxidant enzymes in vivo and had good antioxidant activity. To sum up, a novel acidic polysaccharide (Mw of 1.28 × 106 Da) with antioxidant activity was isolated from S. miltiorrhiza, and its application prospect in the field of medicine and food was preliminarily revealed.

Structural characterization and preventive effect on alcoholic gastric mucosa and liver injury of a novel polysaccharide from Dendrobium officinale.

In this study, a polysaccharide (DOP) with molecular weight of 8.25 × 105 Da and monosaccharide composition of mannose (Man) and glucose (Glc) at a molar ratio of 4.2: 1 was isolated from Dendrobium officinale. The preventive effect on alcoholic gastric mucosa and liver injury of DOP was also investigated. In vitro data exhibited that the IC50 values of 1, 1-diphenyl-2-picrylhydrazy (DPPH) radical scavenging ability and Fe2+ chelating capacity were 2.762 mg/mL and 6.667 mg/mL, respectively. Both the alcoholic gastric mucosal injury (AGMI) and alcoholic liver injury (ALI) animal models were used to investigate the gastrotrophic and hepatoprotective abilities of DOP. After administration of DOP, both gastric mucosal index (TNF-α, IL-6, PGE2, SOD, and MDA) and hepatic indicators (ALT, AST, SOD and MDA) improved compared to non-DOP groups. Histopathological results displayed that the DOP groups improved gastric epithelial defect and inflammatory cell redness caused by AGMI, and decreased vacuolization, hepatocyte necrosis and fibrosis caused by ALI. The results might be related to adjusting inflammatory factors, eliminating free radicals, and inhibiting lipid peroxidation capacities. These results manifested that DOP may be a therapeutic reagent to attenuate alcohol gastric mucosal and liver injury.

Glycyrrhizic Acid Inhibits Core Fucosylation Modification Modulated EMT and Attenuates Bleomycin-Induced Pulmonary Fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a fatal and incurable chronic interstitial lung disease with an unknown etiology. Recent evidence suggests that epithelial-mesenchymal transition (EMT) is one of the possible factors in the pathogenesis of pulmonary fibrosis. Glycyrrhizic acid (GA) is a natural active ingredient extracted from the root of the traditional Chinese herb licorice, which has been shown in previous studies to have the effect of alleviating lung injury. In this study, our objective was to investigate whether GA could ameliorate pulmonary fibrosis by altering EMT, as well as the therapeutic potential of changing core fucosylation (CF) to target EMT-related pathways. First, we verified that GA partially reverses EMT in a rat model of bleomycin-induced lung interstitial fibrosis, alleviating pulmonary fibrosis, and implying that GA has antifibrotic potential. Next, we discovered that GA attenuated lung interstitial fibrosis by reducing CF modifications to some extent. Interestingly, we found that GA therapy reduced the expression of phosphorylated Smad2/3 (p-Smad2/3) and ß-catenin in the EMT pathway and that GA inhibited the modification of TGF-ßR and WNT receptor proteins by CF, suggesting that GA may interfere with the EMT process by modulating TGF-ßR, WNT core fucosylation modifications to attenuate pulmonary fibrosis. In conclusion, these findings indicate that GA could be a potential therapeutic agent for IPF, and further support the idea that targeting CF alterations could be a novel technique for the treatment of diseases involving EMT.

[Removal of bisphenol A and tetrabromobisphenol A membrane by nanofiltration from water source].

The removal efficiency of BPA and TBBPA by nanofiltration membrane Desal 5 DK has been investigated with a lab-scale dead-end filtration module and the role of adsorption of two molecules on membrane was also explored to understand the filtration mechanism. The results showed that the R(obs) of BPA decreased from 89% to 47% as the accumulated adsorption quantity of BPA onto the membrane increased to 30 microg x m(-2). The high BPA concentration in adsorption layer caused the water flux decline especially at high pressure. The high TBBPA rejection of over 95% by Desal 5 DK was obtained due to the molecular weight and molecular structure although the accumulated adsorption quantity of TBBPA reached 50 microg x m(-2). The desorption test showed that the TBBPA could not pass through the membrane for its structure at the 5 x 10(5) Pa, while BPA could diffuse through the membrane and the peak concentration was obtained after 30 mL filtration. The quantity of BPA released from the membrane contributed 30% of the total amount adsorbed by the membrane Desal 5 DK.