Rechargeable aqueous Zn-MnO 2 batteries are a promising candidate for large-scale energy storage systems due to their outstanding advantages, such as high energy density, high safety, low cost, and environmental friendliness. Considering the controversies surrounding the mechanism of this battery containing a mildly acidic electrolyte, the electrochemical behavior of this type of battery using β-MnO 2 as the cathode is systematically investigated. The results indicate that the reversible intercalation of Zn 2+ ions into MnO 2 is not likely to take place in the aqueous system. We conclude that it is the existence of the water molecule and its participation in the electrochemical reactions, for instance, the reversible insertion of proton into MnO 2 and the electrolysis of water, that makes the mechanism of aqueous Zn-MnO 2 batteries complicated. Besides, the capacity fading of this mildly acidic Zn-MnO 2 battery is assigned to the generation of the inert layer of Zn 4 SO 4 (OH) 6 •nH 2 O and the ZnMn 2 O 4 on the cathode via electrochemical conversion reactions, the dissolution of the active material during discharging, and the release of gases. When Mn 2+ ions are available in the electrolyte, they will be electrodeposited on the cathode during charging, and the kinetics of the electrochemical reactions of the electrode is improved, leading to the higher electrochemical performance of the battery.

BackgroundMicroglial activation plays an important role in neurodegenerative diseases through production of nitric oxide (NO) and several pro-inflammatory cytokines. Lipoxins (LXs) and aspirin-triggered LXs (ATLs) are considered to act as 'braking signals' in inflammation. In the present study, we investigated the effect of aspirin-triggered LXA4 (ATL) on infiammatory responses induced by lipopolysaccharide (LPS) in murine microglial BV-2 cells.MethodsBV-2 cells were treated with ATL prior to LPS exposure, and the effects of such treatment production of nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α) were analysed by Griess reaction, ELISA, western blotting and quantitative RT-PCR. Moreover, we investigated the effects of ATL on LPS-induced nuclear factor-κB (NF-κB) activation, phosphorylation of mitogen-activated protein kinases (MAPKs) and activator protein-1 (AP-1) activation.ResultsATL inhibited LPS-induced production of NO, IL-1β and TNF-α in a concentration-dependent manner. mRNA expressions for iNOS, IL-1β and TNF-α in response to LPS were also decreased by ATL. These effects were inhibited by Boc-2 (a LXA4 receptor antagonist). ATL significantly reduced nuclear translocation of NF-κB p65, degradation of the inhibitor IκB-α, and phosphorylation of extracellular signal-regulated kinase (ERK) and p38 MAPK in BV-2 cells activated with LPS. Furthermore, the DNA binding activity of NF-κB and AP-1 was blocked by ATL.ConclusionsThis study indicates that ATL inhibits NO and pro-inflammatory cytokine production at least in part via NF-κB, ERK, p38 MAPK and AP-1 signaling pathways in LPS-activated microglia. Therefore, ATL may have therapeutic potential for various neurodegenerative diseases.

BackgroundMicroglia play key roles in innate immunity, homeostasis, and neurotropic support in the central nervous system. Similar to macrophages, microglia adopt two different activation phenotypes, the classical and alternative activation. Resolvin D1 (RvD1) is considered to display potent anti-inflammatory and pro-resolving actions in inflammatory models. In this present study, we investigate the effect of RvD1 on IL-4-induced alternative activation in murine BV-2 microglial cells.MethodsBV-2 cells were incubated with RvD1 alone, IL-4 alone, or the combination of RvD1 and IL-4. Western blot and immunofluorescence were performed to detect protein levels of alternative activation markers arginase 1 (Arg1), chitinase 3-like 3 (Ym1). Moreover, we investigated the effects of RvD1 on IL-4-induced activation of signal transducer and activators of transcription 6 (STAT6) and peroxisome proliferator-activated receptor gamma (PPARγ).ResultsRvD1 promoted IL-4-induced microglia alternative activation by increasing the expression of Arg1 and Ym1. RvD1 also enhanced phosphorylation of STAT6, nuclear translocation of PPARγ and the DNA binding activity of STAT6 and PPARγ. These effects were reversed by butyloxycarbonyl-Phe-Leu-Phe-Leu-Phe (a formyl peptide receptor 2 antagonist). Further, the effects of RvD1 and IL-4 on Arg1 and Ym1 were blocked by the application of leflunomide (a STAT6 inhibitor) or GW9662 (a PPARγ antagonist).ConclusionsOur studies demonstrate that RvD1 promotes IL-4-induced alternative activation via STAT6 and PPARγ signaling pathways in microglia. These findings suggest that RvD1 may have therapeutic potential for neuroinflammatory diseases.

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In this report, acid-soluble collagen (ASC-MC) and pepsin-soluble collagen (PSC-MC) were extracted from the scales of miiuy croaker (Miichthys miiuy) with yields of 0.64 ± 0.07% and 3.87 ± 0.15% of dry weight basis, respectively. ASC-MC and PSC-MC had glycine as the major amino acid with the contents of 341.8 ± 4.2 and 344.5 ± 3.2 residues/1000 residues, respectively. ASC-MC and PSC-MC had lower denaturation temperatures (32.2 °C and 29.0 °C for ASC-MC and PSC-MC, respectively) compared to mammalian collagen due to their low imino acid content (197.6 and 195.2 residues/1000 residues for ASC-MC and PSC-MC, respectively). ASC-MC and PSC-MC were mainly composed of type I collagen on the literatures and results of amino acid composition, SDS-PAGE pattern, ultraviolet (UV) and Fourier-transform infrared spectroscopy (FTIR) spectra. The maximum solubility of ASC-MC and PSC-MC was appeared at pH 1–3 and a sharp decrease in solubility was observed when the NaCl concentration was above 2%. Zeta potential studies indicated that ASC-MC and PSC-MC exhibited a net zero charge at pH 6.66 and 6.81, respectively. Furthermore, the scavenging capabilities on 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, hydroxyl radical, superoxide anion radical and 2,2′-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid (ABTS) radical of ASC-MC and PSC-MC were positively correlated with their tested concentration ranged from 0 to 5 mg/mL and PSC-MC showed significantly higher activity than that of ASC-MC at most tested concentrations (p < 0.05). In addition, the scavenging capability of PSC-MC on hydroxyl radical and superoxide anion radical was higher than those of DPPH radical and ABTS radical, which suggested that ASC-SC and PSC-SC might be served as hydroxyl radical and superoxide anion radical scavenger in cosmeceutical products for protecting skins from photoaging and ultraviolet damage.

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Lipoxins have emerged as mediators of key events in endogenous anti-inflammation and resolution. However, the implication of these novel lipid mediators on neuroinflammation has not been investigated. Microglia is the major cells involved in brain tissue damage during infection and neurodegenerative diseases. One of the major features shared by neuroinflammation conditions is the increased production of reactive oxygen species (ROS) generated by NADPH oxidase activation. In this study, we have examined whether aspirin-triggered lipoxin A(4) (ATL) modulates ROS generation in BV2 cells. Pre-treatment of BV2 cells with ATL blocked ROS production triggered by LPS in the time-dependent and concentration-dependent manner. ATL inhibited the translocation of the cytoplasmic NADPH oxidase subunit p47(phox) to the cell membrane as well as NADPH oxidase activity. Taken together, these results demonstrate that ATL suppresses NADPH oxidase-mediated ROS generation in BV2 microglia cells, strongly indicating that ATL may play an important role against the development and progression of neuroinflammtion.

For using aquatic by-products to manufacture high-value products, Skipjack tuna (Katsuwonus pelamis) roes were degreased, pretreated with microwave, and hydrolyzed using five proteases. The protein hydrolysate (TRPH) generated using Flavourzyme displayed the strongest 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity. Twelve antioxidative peptides were prepared from TRPH by ultrafiltration and chromatography methods and determined to be SGE, VDTR, AEM, QDHKA, TVM, QEAE, YEA, VEP, AEHNH, QEP, QAEP, and YVM with molecular weights of 291.24, 489.50, 349.41, 597.59, 349.44, 475.42, 381.36, 343.37, 606.58, 372.35, 443.42, and 411.49 Da, respectively. AEM, QDHKA, YEA, AEHNH, and YVM presented the strongest scavenging activity on DPPH radical (EC50 values of 0.250±0.035, 0.279±0.017, 0.233±0.012, 0.334±0.011, and 0.288±0.015 mg/ml, respectively), hydroxyl radical (EC50 values of 0.456±0.015, 0.536±0.021, 0.476 ± 0.051, 0.369 ± 0.052, and 0.413 ± 0.019 mg/ml, respectively), and superoxide anion free radical (EC50 values of 0.348 ± 0.018, 0.281 ± 0.013, 0.305 ± 0.022, 0.198 ± 0.011, and 0.425 ± 0.021 mg/ml, respectively). Moreover, AEM, QDHKA, YEA, AEHNH, and YVM presented high lipid peroxidation inhibition ability, Ferric-reducing power, and significant protective function on H2O2-induced Chang liver cells. Therefore, AEM, QDHKA, YEA, AEHNH, and YVM could be natural antioxidant ingredients used in pharmaceutical and functional products.