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Glyphosate is an herbicide commonly used in agriculture, and its widespread use has adversely affected the survival of nontarget organisms. Among these organisms, bees in particular are important pollinators, and declining bee populations have severely affected crop yields around the world. However, the molecular mechanism by which glyphosate harms bees remains unclear. In our experiment, we screened and cloned a glyphosate-induced gene in Apis cerana cerana (A. c. cerana) and named glyphosate response factor 1 (AccGRF1). Sequence analysis showed that AccGRF1 contains a winged-helix DNA binding domain, which suggests that it belongs to the Forkhead box (Fox) protein family. qRT–PCR and heterologous expression in Escherichia coli and yeast showed that AccGRF1 can respond to glyphosate and oxidative stress. After AccGRF1 knockdown by means of RNA interference (RNAi), the resistance of A. c. cerana to glyphosate stress improved. The results suggested that AccGRF1 is involved in A. c. cerana glyphosate stress tolerance. This study reveals the functions of Fox transcription factors in response to glyphosate stress and provides molecular insights into the regulation of glyphosate responses in honeybees. [Display omitted] • A glyphosate-induced gene (AccGRF1) was screened and identified from bees. • AccGRF1 protein belongs to Forkhead protein family transcription factors. • E. coli and yeast overexpressing AccGRF1 were more sensitive to oxidative stress. • AccGRF1 is involved in oxidative stress response caused by glyphosate in bees. [ABSTRACT FROM AUTHOR]

Clostridioides difficile is a Gram-positive, obligate anaerobic, spore-producing intestinal opportunistic pathogen. CDI outbreaks in Europe and the Americas in recent years are a major health concern. Intestinal short-chain fatty acids (SCFAs) are an important energy source for colonic epithelial cells, and the roles of SCFAs in reducing intestinal inflammation, inhibiting intestinal tumors, and regulating gut microbial homeostasis are being actively researched. Furthermore, SCFAs attenuate CDI or directly inhibit C. difficile growth through different pathways in vivo and in vitro. This review assesses the role of SCFAs in CDI and discusses the potential use of these molecules as therapeutic targets for CDI. • Short-chain fatty acids inhibit Clostridioides difficile infection by enhancing host antibacterial immune response. • Dietary interventions regulate the production of short-chain fatty acids to reduce Clostridioides difficile infection. • The gut microbiota plays a role in regulating gut homeostasis by producing short-chain fatty acids. [ABSTRACT FROM AUTHOR]

Abstract: DNA-binding proteins play a vitally important role in many biological processes. Prediction of DNA-binding proteins from amino acid sequence is a significant but not fairly resolved scientific problem. Chaos game representation (CGR) investigates the patterns hidden in protein sequences, and visually reveals previously unknown structure. Fractal dimensions (FD) are good tools to measure sizes of complex, highly irregular geometric objects. In order to extract the intrinsic correlation with DNA-binding property from protein sequences, CGR algorithm, fractal dimension and amino acid composition are applied to formulate the numerical features of protein samples in this paper. Seven groups of features are extracted, which can be computed directly from the primary sequence, and each group is evaluated by the 10-fold cross-validation test and Jackknife test. Comparing the results of numerical experiments, the group of amino acid composition and fractal dimension (21-dimension vector) gets the best result, the average accuracy is 81.82% and average Matthew's correlation coefficient (MCC) is 0.6017. This resulting predictor is also compared with existing method DNA-Prot and shows better performances. [Copyright &y& Elsevier]

Fractions, bioavailability, health risks of fine particulate maters (PM 2.5)-bound potentially toxic elements (PTEs) (Pb, Cd, Cr, Cu and Zn) were investigated before and after coal limiting in Baoding city. The winter PM 2.5 samples were collected at different functional areas such as residential area (RA), industrial area (IA), suburb (SB), street (ST) and Botanical Garden Park (BG) in 2016 (coal dominated year) and 2017 (gas dominated year). The fractions and bioavailability of PTEs were determined and evaluated based on BCR sequential extraction. Health risks through inhalation exposure were evaluated by US EPA health risk assessment model. The results from different years and functional areas were compared and discussed. The fractions and bioavailability of PM 2.5 -bound PTEs varied with functional areas. The percentages of cadmium (Cd) and zinc (Zn) in acid-soluble fraction (F1–Cd and F1–Zn) to the total amount of Cd and Zn were low in BG samples (p < 0.05). Bioavailability of Cd were high in SB samples (p < 0.05). Total contents of PM-bound PTEs in 2017 generally decreased compared with 2016. The differences of fraction and bioavailability between 2016 and 2017 depended on the elements and areas. Higher proportions of copper (Cu) in acid-soluble fraction (F1–Cu) and bioavailability of Cu (p < 0.05) were found in 2017 samples. Significant differences were found just at IA and RA for Pb, Cd and Zn. Our results indicated that the health risks from inhalation exposure for PTEs in PM 2.5 declined about 11%–52% after the coal limiting in this city. Image 1 • Total concentrations of PTEs in PM 2.5 generally decreased after coal limiting. • The changes of fraction after coal limiting depended on the element and area. • Health risk from inhalation for PTEs in PM 2.5 declined 11–52% after coal limiting. [ABSTRACT FROM AUTHOR]

Abstract The present study was conducted to evaluate the protective effects of astaxanthin against lipopolysaccharide (LPS)-induced inflammatory responses in Channa argus in vivo and ex vivo. Primary hepatocytes were exposed to different concentrations of LPS for 24 h to induce an inflammatory response, and the protective effects of astaxanthin against LPS-induced inflammation were studied ex vivo and in vivo. Hepatocytes exposed to LPS (5–20 μg mL−1) alone for 24 h resulted in a significant increase in lactate dehydrogenase release (LDH), Nitric oxide (NO) production and Malondialdehyde (MDA) content, 10 μg mL−1 LPS could induced inflammatory response in hepatocytes. Gene expression of TLR4, NFkBp65, MAPKp38, TNF-α, IL-6 and IL-1β mRNA expression were also enhanced ex vivo (p < 0.05). In vivo test demonstrated that pretreatment with astaxanthin prevented the LPS-induced upregulation of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β. Besides, astaxanthin blocked the expression of Toll-like receptor 4 (TLR4) and then suppressed the phosphorylation of nuclear transcription factor-kappa B (NF-κB) p65 and degradation inhibitor of NF-κBα (IκBα). Further study showed that astaxanthin could suppress the phosphorylation of p38, extracellular signal-regulated kinase (ERK) and c-jun NH2-terminal kinase (JNK) in mitogen-activated protein kinase (MAPK) signal pathway. In conclusion, our results suggest that astaxanthin played an anti-inflammatory role by regulating TLR4 and the NF-κB and MAPK signaling pathways in C. argus. Highlights • We established LPS induced inflammatory response model in Channa argus hepatocytes in vitro. • Astaxanthin prevented LPS-induced upregulation of pro-inflammatory cytokines and related gene expression. • Astaxanthin attenuates inflammatory responses by suppressing NF-κB and MAPK signaling pathways in Channa argus. [ABSTRACT FROM AUTHOR]

This study was undertaken to isolate active secondary metabolites from immunostimulatory Bacillus Licheniformis XY-52 and evaluate their activities at 0%, 0.5%, 1.0%, and 2.0% doses supplementation with feed on immune response in common carp at weeks 1, 2, and 3. By applying chromatography techniques and successive recrystallization, two purified metabolites were obtained and identified by spectral data (mass spectrometry and nuclear magnetic resonance) as: Cyclo-(Phe–Tyr) and Cyclo-(Phe–Gly). The results revealed that humoral innate immune parameters (lysozyme activity, phagocytic activity and bactericidal activity) were significantly (P < 0.05) increased after feeding on the two active compounds-supplemented diet. Furthermore, administration of the two active compounds significantly (P < 0.05) up regulated IL-1β, Type 1 IFN, IFN g2b, IL10 and TNF-α gene expression. Heat shock protein 70 (HSP70) gene expression was significantly (P < 0.05) lower as compared to control group at the end of trial. Common carp fed with the two compounds had higher survival rates (69.3%) compared to the controls (32.0%) after challenged with the pathogen, Aeromonas hydrophila . The present study indicates that the two isolated active compounds could positively influence immune response and enhance disease resistance of common carp against A. hydrophila infection. [ABSTRACT FROM AUTHOR]

Angiogenesis plays an important role in the growth and metastasis of solid tumors including melanoma. Inhibiting tumor-associated angiogenesis is a tactic in treating melanoma. Dioscin restrains angiogenesis in colon tumor and has anti-melanoma effects in cell and animal models. In a previous study, we found that dioscin inhibits Src/STAT3 signaling in melanoma cells. Activation of the Src/STAT3 pathway has been shown to promote tumor angiogenesis. This study aimed to determine whether dioscin's anti-melanoma effects is related to inhibiting Src/STAT3 signaling-mediated angiogenesis. In a B16F10 allograft mouse model, we found that dioscin inhibited melanoma growth and angiogenesis. To exclude the impact of tumor growth on angiogenesis, a chicken chorioallantoic membrane (CAM) model was used to verify the anti-angiogenic effect of dioscin. Results showed that dioscin suppressed vessel formation in CAM. To determine if tumor secreted pro-angiogenic cytokines are involved in the anti-angiogenic effect of dioscin, conditioned media from dioscin-treated A375 melanoma cells were used to culture human umbilical vein endothelial cells (HUVECs), and tube formation was monitored. It was observed that the tube formation of HUVECs was inhibited. Mechanistic studies revealed that dioscin inhibited the activation of Src and STAT3, and lowered mRNA and protein levels of STAT3 transcriptionally-regulated genes, in B16F10 melanomas. ELISA assays showed that dioscin decreased the secretion of MMP-2, MMP-9 and VEGF from A375 cells. Over-activation of STAT3 lessened the effects of dioscin in decreasing the secretion of pro-angiogenic cytokines from melanoma cells, and in inhibiting tube formation of HUVECs cultured with conditioned media from melanoma cell cultures. In summary, we for the first time demonstrated that inhibiting Src/STAT3 signaling-mediated angiogenesis is involved in the anti-melanoma effects of dioscin. This study provides further pharmacological groundwork for developing dioscin as an anti-melanoma agent. [Display omitted] We used in vitro and in vivo models to investigate the anti-angiogenic effects and mechanisms of dioscin. We demonstrated that inhibiting Src/STAT3 signaling-mediated angiogenesis is associated with the anti-melanoma effects of dioscin. [ABSTRACT FROM AUTHOR]

Abstract: Resveratrol (RES), a natural plant polyphenol, is an effective inducer of cell cycle arrest and apoptosis in a variety of carcinoma cell types. In addition, RES has been reported to inhibit tumorigenesis in several animal models suggesting that it functions as a chemopreventive and anti-tumor agent in vivo. The chemopreventive and chemotherapeutic properties associated with resveratrol offer promise for the design of new chemotherapeutic agents. However, the mechanisms by which RES mediates its effects are not yet fully understood. In this study, we showed that RES caused cell cycle arrest and proliferation inhibition via induction of unfolded protein response (UPR) in human leukemia K562 cell line. Treatment of K562 cells with RES induced a number of signature UPR markers, including transcriptional induction of GRP78 and CHOP, phosphorylation of eukaryotic initiation factor 2α (eIF2α), ER stress-specific XBP-1 splicing, suggesting the induction of UPR by RES. RES inhibited proliferation of K562 in a concentration-dependent manner. Flow cytometric analyses revealed that K562 cells were arrested in G1 phase upon RES treatment. Salubrinal, an eIF2α inhibitor, or overexpression of dominant negative mutants of PERK or eIF2α, effectively restored RES-induced cell cycle arrest, underscoring the important role of PERK/eIF2α branch of UPR in RES-induced inhibition of cell proliferation. [Copyright &y& Elsevier]

Selenium (Se) is a micronutrient that becomes toxic when present at higher concentrations in fish tissues. Allium mongolicum Regel flavonoids (AMRF) have been documented to possess antioxidant, immunoenhancement and anti-inflammation properties. The aim of this study was to investigate the protective effects and potential mechanisms of dietary supplementation of AMRF and Se exposure on oxidative stress, immune responses and immune-related genes expression in Channa argus. A total of 480 C. argus were randomly divided into eight groups housed in twenty-four 200 L glass aquarium (3 tanks per group, 20 fish per tank). The fish were exposed for 56 days to waterborne Se at 0, 50, 100 and 200 μg/L and/or dietary AMRF at 40 mg/kg. The result indicated that AMRF exerted significant protective effects by preventing alterations in the levels of bioaccumulation, malondialdehyde, lysozyme, complement C3 and immunoglobulin M. AMRF also assists in the elevation of catalase and glutathione peroxidase in the liver and spleen while regulating the expression of immune-related genes including NF-κB p65, IκB-α, TNF-α, IL-1β, IL-8, HSP70, HSP90, and glucocorticoid receptor after 56 days of Se exposure. Our results suggest that administration of AMRF (40 mg/kg) has the potential to combat Se toxicity in C. argus. • Exposure to waterborne Se induced significant bioaccumulation in specific tissues. • Antioxidant and immune responses were affected following exposure to waterborne Se. • AMRF supplementation effectively attenuated Se-induced toxicity. [ABSTRACT FROM AUTHOR]

Abstract Three 3D Cd(II) complexes, namely, {[Cd 4 (L) 2 (dioxane) 3 (H 2 O) 3 ]·DMA·5H 2 O} n (1), {[Cd 2 (L)(phen)(H 2 O) 3.5 ]·4H 2 O} n (2) and {[Cd 2 (L)(phen)(H 2 O) 4 ]·3H 2 O·DMA} n (3) have been synthesized from the ligand of 3,5-di(2′,5-dicarboxylphenyl)pyridine (H 4 L) with or without the assistance of phen auxiliary linker (phen = 1,10-phenanthroline). Complex 1 displays a 3D (4,4,9)-connected net with the point symbol of {3.45}{32.414.55.611.72.82}{45.6}. Complex 2 shows a 3D (4,8)-connected net with the point symbol of {43. 63} 2 {46.619.83}. Complex 3 presents a 3D 4-connected net with the point symbol of {43.62.8}. The fluorescence measurements showed 1 – 3 exhibit sensitive detection of Fe(III) and Cr(VI) ions with a low detection limit. In addition, the gas sorption isotherms of complex 3 for N 2 , H 2 , CO 2 and CH 4 were investigated, and the corresponding uptakes are 239.8 cm3 g−1 for N 2 and 93.9 cm3 g−1 for H 2 at 77 K, 50.5 cm3 g−1 for CO 2 and 17.0 cm3 g−1 for CH 4 at 298 K, 54.8 cm3 g−1 for CO 2 and 24.2 cm3 g−1 for CH 4 at 273 K, respectively. Based on the N 2 isotherm, the Brunauer−Emmett−Teller (BET) and Langmuir surface area of 3 were calculated to be 610.1 and 710.5 m2 g−1, respectively. Moreover, the two binary gas mixtures adsorption was also studied, indicating that the adsorption of 3 for CO 2 is better than that of CH 4 , which was verified by ideal adsorbed solution theory (IAST) with the adsorption selectivity being 8.5 (landfill gas, CO 2 /CH 4 = 0.5/0.5) and 7.2 (natural gas, CO 2 /CH 4 = 0.05/0.95). Graphical abstract Three 3D Cd(II) complexes have been synthesized from the ligand of 3,5-di(2′,5-dicarboxylphenyl)pyridine (H 4 L) with or without the assistance of phen auxiliary linker (phen = 1,10-phenanthroline). For complexes 1 – 3 , the fluorescence measurements were studied, exhibiting sensitive detection of Fe(III) and Cr(VI) ions. In addition, the gas sorption isotherms of complex 3 for N 2 , H 2 , CO 2 and CH 4 were investigated. fx1 Highlights • Three Cd(II) complexes have been constructed from 3,5-di(2′,5-dicarboxylphenyl)pyridine (H 4 L) with or without the help of phen. • In addition, luminescent properties of complexes, the adsorption behaviors and the selectivity of 3 for CO 2 /CH 4 separation were investigated. [ABSTRACT FROM AUTHOR]

Abstract: Lipopolysaccharide (LPS) is an outer-membrane glycolipid component of Gram-negative bacteria known for its fervent ability to activate monocytic cells and for its potent proinflammatory capabilities. Bcl-2-associated athanogene 3 (BAG3) is a survival protein that has been shown to be stimulated during cell response to stressful conditions, such as exposure to high temperature, heavy metals, proteasome inhibition, and human immunodeficiency virus 1 (HIV-1) infection. In addition, BAG3 regulates replication of Varicella–Zoster Virus (VZV) and Herpes Simplex Virus (HSV) replication, suggesting that BAG3 could participate in the host response to infection. In the current study, we found that LPS increased the expression of BAG3 in a dose- and time-dependent manner. Actinomycin D completely blocked the LPS-induced BAG3 accumulation, as well as LPS activated the proximal promoter of BAG3 gene, supported that the induction by LPS occurred at the level of gene transcription. LPS-induced BAG3 expression was blocked by JNK or NF-κB inhibition, suggesting that JNK and NF-κB pathways participated in BAG3 induction by LPS. In addition, we also found that induction of BAG3 was implicated in monocytic cell adhesion to extracellular matrix induced by LPS. Overall, the data support that BAG3 is induced by LPS via JNK and NF-κB-dependent signals, and involved in monocytic cell-extracellular matrix interaction, suggesting that BAG3 may have a role in the host response to LPS stimulation. [Copyright &y& Elsevier]

In order to obtain the porcine recombinant visfatin protein with high expression and low endotoxin content, the current study aims to express and verify the biological activity of the purified porcine recombinant visfatin protein. Firstly, four different expression strains were successfully constructed. Then they were simultaneously induced at 37 °C for 4 h and 16 °C for 16 h. The results showed that Visfatin-pET28a-Transetta was the best strain with high protein expression and purity at 16 °C induction for 16 h. After that, endotoxin was reduced from the recombinant visfatin until the residual endotoxin was less than one endotoxin units per milliliter (EU/mL). Finally, the purified porcine recombinant visfatin protein was incubated with RAW264.7 cells. The results of cell counting kit-8 (CCK-8) showed the survival rate of the cells first increased and then decreased with the increase in visfatin concentration. When the concentration of visfatin was 700 ng/mL, the survival rate of the cells was the highest. Thereafter, control (PBS), Visfatin and Visfatin + PolymyxinB (Ploy.B) groups were incubated with the RAW264.7 cells for 6 h. Real-time quantitative polymerase chain reaction (RT-qPCR) and Enzyme Linked Immuno-Sorbent Assay (ELISA) results showed that, as compared to the control group, the expressions of interleukin (IL)-1β, tumor necrosis factor (TNF)-α and monocyte chemoattractant protein (MCP)-1 in Visfatin group were significantly increased (P < 0.05). However, there was no significant difference between the Visfatin and Visfatin + Poly.B groups, indicating that porcine recombinant visfatin protein promoted the inflammatory activity of RAW264.7 cells while the residual endotoxin did not play a role, suggesting biological activity of porcine recombinant visfatin protein. • Successful construction of four different prokaryotic expression strains. • Preparation of porcine recombinant visfatin with low endotoxin content and high biological activity. • Porcine recombinant visfatin promoted the inflammatory activity of RAW264.7 cells. • The above results proved the biological activity of porcine recombinant visfatin. [ABSTRACT FROM AUTHOR]