Zhou Song

Huazhong University of Science and Technology, Wu-han-shih, Hubei, China

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Publications (11)23.88 Total impact

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    ABSTRACT: Silver bismuth oxide(BSO) was prepared by a simple ion exchange-coprecipitation method with AgNO3 and NaBiO, .2H2O as raw materials, and then used to oxidatively degrade tetrabromobisphenol A(TBBPA). Effects of the molar ratio of Ag/Bi during BSO preparation and the BSO dosage on the degradation of TBBPA were investigated. The results showed that under the optimized conditions (i.e., the Ag/Bi molar ratio of 1:1, BSO dosage of 1 g x L(-1), 40 mg x L(-1) of TBBPA was completely degraded and the removal of total organic carbon achieved more than 80% within 7 min. The degradation intermediates of TBBPA were identified by ion chromatography, gas chromatograph-mass spectrometer and X-ray photoelectron spectroscopy. The degradation pathway of TBBPA included the debromination, the cleavage of tert-butyl group and the open epoxidation of benzene ring. Based on a quenching study of NaN3, singlet oxygen was proved to play a dominant role in the TBBPA degradation.
    Huan jing ke xue= Huanjing kexue / [bian ji, Zhongguo ke xue yuan huan jing ke xue wei yuan hui "Huan jing ke xue" bian ji wei yuan hui.] 01/2015; 36(1):209-14. DOI:10.13227/j.hjkx.2015.01.027
  • Zhou Song · Heqing Tang · Nan Wang · Xiaobo Wang · Lihua Zhu ·

    09/2014; 3(3):185-197. DOI:10.12989/aer.2014.3.3.185
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    ABSTRACT: Avian pathogenic Escherichia coli (APEC) are extra-intestinal pathogenic E. coli, and usually cause avian septicemia through breaching the blood-gas barrier. Type II pneumocytes play an important role of maintaining the function of the blood-gas barrier. However, the mechanism of APEC injuring type II pneumocytes remains unclear. α-cyperone can inhibit lung cell injury induced by Staphylococcus aureus. In order to explore whether α-cyperone regulates the adherence and invasion of APEC-O78 to chicken type II pneumocytes, we successfully cultured chicken type II pneumocytes. The results showed that α-cyperone significantly decreased the adherence of APEC-O78 to chicken type II pneumocytes. In addition, α-cyperone inhibited actin cytoskeleton polymerization induced by APEC-O78 through down regulating the expression of Nck-2, Cdc42 and Rac1. These results provide new evidence for the prevention of colibacillosis in chicken.
    Veterinary Immunology and Immunopathology 05/2014; 159(1-2). DOI:10.1016/j.vetimm.2014.02.005 · 1.54 Impact Factor
  • Zhou Song · Heqing Tang · Nan Wang · Lihua Zhu ·
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    ABSTRACT: A method for reductive degradation of perfluorooctanoic acid (PFOA) was established by using a sulfite/UV process. This process led to a PFOA removal of 100% at about 1h and a defluorination ratio of 88.5% at reaction time of 24h under N2 atmosphere, whereas the use of either UV irradiation or SO3(2-) alone induced little defluorination of PFOA under the same conditions. It was confirmed that the reductive defluorination of PFOA was achieved by hydrated electrons being generated from the photo-conversion of SO3(2-) as a mediator. Theoretical reaction kinetic analysis demonstrated that the generation of hydrated electrons was promoted by increasing either SO3(2-) concentration or solution pH, leading to the acceleration of the PFOA defluorination. Accompanying the reduction of PFOA, a small amount of short-chain perfluorocarboxylic acids, less fluorinated carboxylic acids and perfluorinated alkyl sulfonates were generated, all of which were able to be further degraded with further releasing of fluoride ions. Based on the generation, accumulation and distribution of intermediates, hydrated electrons induced defluorination pathway of PFOA was proposed in a sulfite-mediated UV photochemical system.
    Journal of hazardous materials 08/2013; 262C:332-338. DOI:10.1016/j.jhazmat.2013.08.059 · 4.53 Impact Factor
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    ABSTRACT: Abstract In the previous study, we found that peimine has good anti-inflammatory effects in vivo. However, the anti-inflammatory mechanism of peimine remains unclear. We, therefore, assessed the effects of peimine on inflammatory cytokines in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. We found that peimine (0-25 mg/L) significantly inhibited tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and increased IL-10 production. Furthermore, peimine significantly inhibited the phosphorylation of p38, ERK and c-jun N-terminal kinase (JNK) as well as decreased p65 and IκB. The present results indicate that peimine inhibits the production of inflammatory cytokines induced by LPS through blocking MAPKs and NF-κB signaling pathways.
    Immunopharmacology and Immunotoxicology 08/2013; 35(5). DOI:10.3109/08923973.2013.822508 · 1.20 Impact Factor
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    ABSTRACT: Ginsenoside Rh2 is one of the most important ginsenosides in ginseng with anti-inflammatory and antitumor effects. However, the extremely poor oral bioavailability induced by its low water solubility greatly limits the potency of Rh2 in vivo. In the previous study, we sulfated 20(S)-ginsenoside Rh2 with chlorosulfonic acid and pyridine method, and got one novel derivative, Rh2-B1, with higher water solubility and greater immunologic enhancement than Rh2. However, the anti-inflammatory effect of Rh2-B1 remains unclear. We therefore investigated the effects of Rh2-B1 on lipopolysaccharide (LPS)-induced proinflammatory mediators in RAW 264.7 macrophages. We found that Rh2-B1 dramatically inhibited LPS-induced overproduction of nitric oxide, prostaglandin E2, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. Consistently, the protein and mRNA expression levels of inducible nitric oxide synthase and cyclooxygenase-2 were remarkably decreased by Rh2-B1. In addition, Rh2-B1 significantly suppressed the phosphorylations of p38, c-Jun N-terminal kinase, and extracellular signal receptor-activated kinase 1/2 induced by LPS. Rh2-B1 was further shown to inhibit NF-κB p65 translocation into the nucleus by suppressing IκBα degradation. In conclusion, we demonstrate that Rh2-B1 inhibits the release of LPS-induced pro-inflammatory mediators through blocking mitogen-activated protein kinases and NF-κB signaling pathways, suggesting that sulfated ginsenosides could be potential agents for anti-inflammatory therapies.
    European journal of pharmacology 05/2013; 712(1). DOI:10.1016/j.ejphar.2013.04.036 · 2.53 Impact Factor
  • Junjian An · Lihua Zhu · Nan Wang · Zhou Song · Zeyu Yang · Dongyun Du · Heqing Tang ·
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    ABSTRACT: GrapheneBiFeO3 nanoscaled composites were prepared with a sol–gel method and evaluated as highly efficient photo-Fenton like catalyst under visible light irradiation. The grapheneBiFeO3 composite had a specific surface area of 35.07 m2 g−1, being considerably larger than that of BiFeO3 nanoparticles (7.50 m2 g−1). The composite exhibited excellent visible light-Fenton like catalysis activity, being influenced by calcination temperature, graphene content and solution pH value. Under optimal conditions with visible light irradiation, the grapheneBiFeO3 composite yielded fast degradation of tetrabromobisphenol A with a apparent rate constant of 1.19 min−1, which was 5.43 and 3.68 folds of that achieved by using BiFeO3 and the mixture of BiFeO3 and graphene, respectively. The significantly enhanced visible light-Fenton like catalytic properties of the grapheneBiFeO3 composite in comparison with that of BiFeO3 was attributed to a large surface area, much increased adsorption capacity and the strong electron transfer ability of graphene in the composite.
    The Chemical Engineering Journal 03/2013; 219:225–237. DOI:10.1016/j.cej.2013.01.013 · 4.32 Impact Factor
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    ABSTRACT: Xiang-Qi-Tang (XQT) is a Chinese herbal formula containing Cyperus rotundus, Astragalus membranaceus, and Andrographis paniculata. Alpha-Cyperone (CYP), astragaloside IV (AS-IV), and andrographolide (AND) are the three major active components in this formula. XQT may modulate the inflammatory or coagulant responses. We therefore assessed the effects of XQT on lipopolysaccharide (LPS)-induced inflammatory model of rat cardiac microvascular endothelial cells (RCMECs). XQT, CYP, AS-IV, and AND inhibited the production of tumor necrosis factor alpha (TNF-α), intercellular cell adhesion molecule-1 (ICAM-1), and plasminogen activator inhibitor-1 (PAI-1), and up-regulated the mRNA expression of Kruppel-like factor 2 (KLF2). XQT and CYP inhibited the secretion of tissue factor (TF). To further explore the mechanism, we found that XQT, or its active components CYP, AS-IV, and AND significantly inhibited extracellular signal-regulated kinase (ERK), c-jun NH2-terminal kinase (JNK), and p38 phosphorylation protein expression as well as decreased the phosphorylation levels of nuclear factor κB (NF-κB) p65 proteins in LPS-stimulated RCMECs. These results suggested that XQT and its active components inhibited the expression of inflammatory and coagulant mediators via mitogen-activated protein kinase (MAPKs) and NF-κB signaling pathways. These findings may contribute to future research on the action mechanisms of this formula, as well as therapy for inflammation- or coagulation-related diseases.
    Immunopharmacology and Immunotoxicology 11/2012; 35(2). DOI:10.3109/08923973.2012.744034 · 1.20 Impact Factor
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    ABSTRACT: The alpha melanocyte stimulating hormone receptor (MC1R) is one of five G-protein coupled receptors belonging to the melanocortin subfamily, MC1R gene has been known to play a major role in regulating of fur color in mammals, and α-MSH and ACTH are endogenous nonselective agonists for MC1R. However, we found that MC1R was highly expressed in Raw 264.7 cells which were important inflammatory cells involved in the initiation of inflammatory responses. In addition, Cyclic AMP is not only a key molecule in the MC1R signal transduction pathway, but dampen innate immune-mediated responses. These intriguing biological results triggered the further conformation studies; it suggested that MC1R was very likely to be an important role in immunoregulation. In this study, we were to investigate the immunosuppressive effects of MC1R on inflammation in lipopolysaccharide (LPS) stimulated Raw 264.7 cells and LPS induced vivo 2-chloro-1,3,5-trinitrobenzene (TNCB)-induced atopic dermatitis (AD) model. The effects of the MC1R antagonist psoralen on pro-inflammatory cytokines and signaling pathways were analyzed by enzyme-linked immunosorbent assay, western blot, real-time fluorescence quantitative PCR and Histological analysis. Our results show a consistent and marked effect of high concentrations of MC1R antagonist psoralen increased the level of MC1R mRNA in Raw 264.7 cells by cumulative feedback regulation through preferential binding of MC1R. Moreover, as evidenced by inhibiting the LPS-induced TNF-α, IL-6 and enhancing the expression level of cyclic AMP protein in vitro. In vivo study it was also observed that psoralen promoted on histopathologic changes in the skin tissue of TNCB-induced AD mice. Taken together, our results suggest that MC1R decrease the inflammation in vitro and vivo, and might be a therapeutic signaling pathway to against inflammatory diseases.
    Molecular Biology Reports 10/2012; 40(2). DOI:10.1007/s11033-012-2256-x · 2.02 Impact Factor
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    ABSTRACT: The degradation of triclosan was investigated in the presence of H2O2 as oxidant and BiFeO3 magnetic nanoparticles (BiFeO3 MNPs) as catalyst at pH 6.0 and room temperature. It was found that the alone addition of H2O2 (10.0 mmol L−1) induced little degradation of the added triclosan (34.5 μmol L−1) after reaction time of 180 min, but the use of BiFeO3 MNPs (0.5 g L−1) increased the triclosan removal to 82.7% in the presence of H2O2. The degradation of triclosan was accompanied by considerable generation and accumulation of carcinogenic 2,4-dichlorophenol. The surface modification of BiFeO3 MNPs by organic ligands such as EDTA was used to enhance the catalytic ability of BiFeO3 MNPs. The addition of EDTA (0.5 mmol L−1) into the triclosan–H2O2–BiFeO3 MNPs system not only resulted in almost complete degradation of the added triclosan within 30 min, but also greatly inhibited the accumulation of the toxic intermediate 2,4-dichlorophenol. The kinetics was clarified for the green catalytic degradation of triclosan in the investigated systems.
    The Chemical Engineering Journal 08/2012; s 198–199:379–387. DOI:10.1016/j.cej.2012.05.067 · 4.32 Impact Factor
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    ABSTRACT: In the previous study, we found that sulfated derivative B2 of ginsenoside Rh2 (Rh2-B2) has greater anti-inflammatory effects than 20(S)-ginsenoside Rh2. However, the anti-inflammatory mechanism of Rh2-B2 remains unclear. We therefore assessed the effects of Rh2-B2 on inflammatory cytokines in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. We found that Rh2-B2 (1-5 mg/L) significantly inhibited tumor necrosis factor alpha, interleukin (IL)-6, IL-1β, and increased IL-10 production from protein and mRNA levels. Furthermore, Rh2-B2 significantly inhibited the phosphorylation of p38 and c-Jun N-terminal kinase as well as decreased p65 nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) translocation into the nucleus by nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha degradation. The present results indicate that Rh2-B2 inhibits the production of inflammatory cytokines induced by LPS through blocking mitogen-activated protein kinases and NF-κB signaling pathways.
    Inflammation 05/2012; 35(5):1659-68. DOI:10.1007/s10753-012-9482-1 · 2.21 Impact Factor

Publication Stats

66 Citations
23.88 Total Impact Points


  • 2012-2015
    • Huazhong University of Science and Technology
      • Department of Chemical Engineering
      Wu-han-shih, Hubei, China
  • 2012-2014
    • Jilin University
      • • Department of Clinical Medicine
      • • College of Animal Science and Veterinary Medicine
      Yung-chi, Jilin Sheng, China