[Preparation of Iron-modified Biochar and Its Application in Arsenic Contaminated Soil Remediation].

Biochar has a range of advantages including large porosity, high specific surface area, and strong adsorption capacity. It has been widely used in environmental pollution remediation, soil improvement, and carbon sequestration and emission reduction. Arsenic (As) is a highly toxic pollutant widely distributed throughout the soil. In typical surface soils, the most common forms of As are arsenite (AsO33-) and arsenate (AsO43-). Since most biochar surfaces are negatively charged, the adsorption efficiency of biochar to arsenic is usually low, and the biochar material needs to be modified to enhance its As adsorption performance. Iron-based materials, such as zero valent iron and iron oxide, are excellent As adsorption materials with wide environmental sources. They can be loaded to biochar to form iron-modified biochar via precipitation, pyrolysis, ball-milling, and micro-biological methods. The combined advantages of the iron-modified biochar will expand the application of biochar materials in environmental remediation. Based on a systematic analysis of the literature on iron-modified biochar in recent years, this study reviewed the common preparation methods of iron-modified biochars; analyzed biochar substrates, iron-modified biochar, and their synergistic mechanisms on As adsorption; and briefly expounded the application status of iron-modified biochar in soil pollution remediation. The prospects of the future research direction of iron-modified biochar were put forward as a reference for the large-scale application of biochar materials in the future.

Circular RNA circ_0000423 promotes gastric cancer cell proliferation, migration and invasion via the microR-582-3p/Disheveled-Axin domain containing 1 axis.

For humans, gastric cancer (GC) is a common malignancy. Multiple circular RNAs (circRNAs) have been confirmed to be important cancer-promoting or tumor-suppressive factors. The present study discusses the roles and mechanisms of circ_0000423 in GC development. In this study, circ_0000423 expression in GC patient tissue samples and cell lines was detected via quantitative real-time polymerase chain reaction. Disheveled-Axin domain containing 1 (DIXDC1) expression in GC cells was examined via Western blot. Besides, cell counting kit-8 was utilized for detecting GC cell viability. GC cell migration and invasion were examined through Transwell assays. Bioinformatics and dual-luciferase reporter gene assays were employed to verify the regulatory relationships between microRNA-582-3p (miR-582-3p) and circ_0000423 or DIXDC1. In the present study, we demonstrated that circ_0000423 was highly expressed in GC. Circ_0000423 knockdown suppressed GC cell viability, migration and invasion. Moreover, miR-582-3p was confirmed as a direct target of circ_0000423, and an upstream regulator of DIXDC1. MiR-582-3p inhibition or DIXDC1 overexpression could reverse the above-mentioned effects of knocking down circ_0000423 on GC cells. In conclusion, circ_0000423 facilitates GC progression by modulating the miR-582-3p/DIXDC1 axis.

[Network pharmacological analysis and experimental study of Pulsatilla chinensis against inflammatory injury caused by pneumonia in mice infected with influenza virus FM_1].

Network pharmacology and the mouse model of viral pneumonia caused by influenza virus FM_1 were employed to explore the main active components and the mechanism of Pulsatilla chinensis against the inflammatory injury of influenza virus-induced pneumonia. The components and targets of P. chinensis were searched from TCMSP, and the targets associated with influenza virus-induced pneumonia were searched from GeneCards. The common targets between P. chinensis and influenza virus-induced pneumonia were identified with Venn diagram established in Venny 2.1. The herb-component-disease-target(H-C-D-T) network was constructed by Cytoscape 3.7.2. The above data were imported into STRING for PPI network analysis. Gene Ontology(GO) enrichment and KEGG pathway enrichment were performed with DAVID. BALB/cAnN mice were infected with the influenza virus FM_1 by nasal drip to gene-rate the mouse model of pneumonia. Immunohistochemistry was adopted to the expression profiling of inflammatory cytokines in the lung tissues of mice in the blank group, model group, and P. chinensis group 1, 3, 5, and 7 days after infection. The pathological changes of lung and trachea of mice in blank group, model group, and P. chinensis group were observed with light microscope and scanning electron microscope at all the time points. The network pharmacological analysis indicated that 9 compounds of P. chinensis were screened out, with a total of 57 targets, 22 of which were overlapped with those of influenza virus-induced pneumonia. A total of 112 GO terms(P<0.05) were enriched, including 81 terms of biological processes, 11 terms of cell components, and 20 terms of molecular functions. A total of 53 KEGG signaling pathways(P<0.05) were enriched, including TNF signaling pathway, influenza A signaling pathway, NF-κB signaling pathway, MAPK signaling pathway and other signaling pathways related to influenza/inflammation. In the P. chinensis group, the expression of TNF-α and IL-1 in the lung tissue was down-regulated on the 3 rd day after infection, and that of IL-6 in the lung tissue was down-regulated on the 5 th day after infection. Light microscopy and scanning electron microscopy showed that P. chinensis significantly alleviated the pathological damage of lung and trachea compared with the model group. This study reflects the multi-components, multi-targets, and multi-pathways of P. chinensis against influenza virus-induced pneumonia. P. chinensis may reduce the production of proinflammatory cytokines and mediators and block the pro-inflammatory signaling pathways to alleviate viral pneumonia, which provides reference for future research.

[Application of numerical taxonomy in study of Dao-di herbs and their producing areas].

As a treasure of traditional Chinese medicine culture,Dao-di herbs are famous for their high quality and good effect.However,traditional characteristics of Dao-di herbs and their producing areas are mostly confined to qualitative description,lacking objective evaluation indicators. Numerical taxonomy,which uses mathematical methods to improve the research of taxonomy from qualitative description to quantitative comprehensive analysis,is objective and accurate,so is widely used in the field of biology and medicine.This paper reviews the concept and main research fields of numerical taxonomy,and summarizes its application status and development prospects in the study of Dao-di herbs and characteristics of production areas,in order to lay the foundation for the objectification and standardization of Dao-di herbs.

Hydrogen sulfide treatment promotes glucose uptake by increasing insulin receptor sensitivity and ameliorates kidney lesions in type 2 diabetes.

AIMS: To examine if hydrogen sulfide (H2S) can promote glucose uptake and provide amelioration in type 2 diabetes. RESULTS: Treatment with sodium hydrosulfide (NaHS, an H2S donor) increased glucose uptake in both myotubes and adipocytes. The H2S gas solution showed similar effects. The NaHS effects were blocked by an siRNA-mediated knockdown of the insulin receptor (IR). NaHS also increased phosphorylation of the IR, PI3K, and Akt. In Goto-Kakizaki (GK) diabetic rats, chronic NaHS treatment (30 µmol·kg(-1)·day(-1)) decreased fasting blood glucose, increased insulin sensitivity, and increased glucose tolerance with increased phosphorylation of PI3K and Akt in muscles. Similar insulin-sensitizing effects of NaHS treatment were also observed in Wistar rats. Moreover, glucose uptake was reduced in the cells with siRNA-mediated knockdown of the H2S-generating enzyme cystathionine γ-lyase in the presence or absence of exogenous H2S. Moreover, chronic NaHS treatment reduced oxygen species and the number of crescentic glomeruli in the kidney of GK rats. INNOVATION AND CONCLUSION: This study provides the first piece of evidence for the insulin-sensitizing effect of NaHS/H2S in the both in vitro and in vivo models of insulin resistance. REBOUND TRACK: This work was rejected during a standard peer review and rescued by the Rebound Peer Review (Antoxid Redox Signal 16: 293-296, 2012) with the following serving as open reviewers: Jin-Song Bian, Samuel Dudley, Hideo Kimura, and Xian Wang.

Hydrogen sulphide inhibits cardiomyocyte hypertrophy by up-regulating miR-133a.

Hydrogen sulphide (H(2)S) has been shown to play a crucial role in cardiovascular physiology and disease. However, there is no information about the possible role of H(2)S in cardiomyocyte hypertrophy (CH). Our results showed that pretreatment with NaHS, an H(2)S donor, significantly reduced [(3)H]-leucine incorporation, cell surface area, mRNA expression of brain natriuretic peptide (BNP), intracellular reactive oxygen species (ROS), miR-21 and increased atrial natriuretic peptide (ANP) and miR-133a expression in hypertrophic cardiomyocytes. Anti-miR133a inhibitor transfection partly reduced the anti-hypertrophic effect of NaHS. In conclusion, H(2)S is a direct inhibitor of CH; it acts by increasing miR-133a and inhibiting the increase in intracellular ROS.

[Inhibitory effect of hydrogen sulfide on cardiac fibroblast proliferation].

The aim of the present study was to investigate the role of hydrogen sulfide (H(2)S) in the proliferation of neonatal rat cardiac fibroblasts (NRCFs). Proliferation of NRCFs was induced by the presence of fetal bovine serum (FBS) or angiotensin II (Ang II) at various concentrations. The concentration-dependent effect of NaHS (donor of H(2)S) on NRCFs proliferation was examined. NRCFs proliferation was assessed by 5'-bromo-2'-deoxyuridine (BrdU) incorporation method. Reactive oxygen species (ROS) level was measured using the dye probe, 2', 7'-dichlorofluorescein diacetate (DCFH-DA). The results showed that FBS- or Ang II-induced NRCFs proliferations were inhibited with the treatment of relatively high concentrations of NaHS (5 × 10(-5) mol/L, 1 × 10(-4) mol/L), but FBS-induced proliferation was increased by low concentration of NaHS (1 × 10(-5) mol/L). Two or 6 h of Ang II (1 × 10(-7) mol/L) treatment caused an increase of ROS level in NRCFs, while this increase was inhibited with NaHS (1 × 10(-4) mol/L) treatment. These results suggest that H(2)S is an inhibitor of cardiac fibroblast at a certain concentration range. This inhibitory effect may be mediated by a reduction in intracellular ROS production.