23 research outputs found

    Development of an enzymeless/mediatorless glucose sensor using ruthenium oxide-Prussian blue combinative analogue

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    Presented in this work is the first step towards an enzymeless/mediatorless glucose sensor. We first observed remarkable electrocatalytic oxidation of glucose using combinative ruthenium oxide (RuOx)-Prussian blue (PB) analogues (designated as mvRuOx-RuCN, mv: mixed valent) at ca. 1.1 V (vs. Ag/AgCl) in acidic media (pH 2 Na2SO4/ H2SO4). Individual RuOx and PB analogs failed to give any such catalytic response. A high ruthenium oxidation state (i.e., oxy/hydroxy-Ru-vii, Edegrees approximate to 1.4 V vs. RHE), normally occurring in strong alkaline conditions at RuOx-based electrodes, was electrogenerated and stabilized (without any conventional disproportionation reaction) in the mvRuOx-RuCN matrix for glucose catalysis. Detail X-ray photoelectron spectroscopic studies can fully support the observation. The catalyst was chemically modified onto a disposable screen-printed carbon electrode and employed for the amperometric detection of glucose via flow injection analysis (FIA). This system has a linear detection range of 0.3 - 20 mM with a detection limit and sensitivity of 40 muM (S/N = 3) and 6.2 muA/(mM cm(2)), respectively, for glucose. Further steps towards the elimination of interference and the extendibility to neutral pHs were addressed

    Trilinolein Inhibits Proliferation of Human Non-Small Cell Lung Carcinoma A549 Through the Modulation of PI3K/Akt Pathway

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    Trilinolein has been identified as one of the active constituents isolated from Panax notoginseng used widely in traditional Chinese medicine. Protective actions of Panax notoginseng against cerebral ischemia, beneficial effects on the cardiovascular system, and hemostatic, antioxidant, hypolipidemic, hepatoprotective, renoprotective and estrogen-like activities have been illustrated. In the present study, the effects of trilinolein on the growth of non-small cell lung carcinoma A549 were investigated. It was found that the exposure of A549 cells to trilinolein resulted in the growth inhibition and the induction of apoptosis in a dose- and time- dependent manner. Trilinolein treatment induced the upregulation of proapoptotic Bax, downregulation of anti-apoptotic Bcl-2 expression, which was associated with the proteolytic activation of caspases and the concomitant degradation of poly(ADP-ribose) polymerase (PARP) protein. Intracellular reactive oxygen species seem to play a role in the trilinolein-induced apoptosis, since ROS were produced early in the trilinolein treatment. Moreover, the activity of PI3K/Akt was downregulated in trilinolein-treated cells. Our results demonstrated that the most important regulators of trilinolein-induced apoptosis are Bcl-2 family and caspase-3, which are associated with cytochrome c release and dephosphorylation on the Akt signaling pathway

    Molecular mechanism of green microalgae, Dunaliella sauna, involved in attenuating balloon injury-induced neointimal formation

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    The pathological mechanism of restenosis is primarily attributed to excessive proliferation of vascular smooth muscle cells (VSMC). The preventive effects of ethanol extract of Dunaliella salina (EDS) on balloon injury-induced neointimal formation were investigated. To explore its molecular mechanism in regulating cell proliferation, we first showed that EDS markedly reduced the human aortic smooth muscle cell proliferation via the inhibition of 5'-bromo-2'-deoxyuridine (BrdU) incorporation at 40 and 801 mu g/ml. This was further supported by the G(0)/G(1)-phase arrest using a flow cytometric analysis. In an in vivo study, EDS at 40 and 80 mu g/ml was previously administered to the Sprague Dawley rats and found that the thickness of neointima, and the ratio of neointima:media were also reduced. EDS inhibited VSMC proliferation in a dose-dependent manner following stimulation of VSMC cultures with 15% fetal bovine serum (FBS). Suppressed by EDS were 15% FBS-stimulated intracellular Rat, phosphorylated extracellular signal-regulated kinases (p-Erk) involved in cell-cycle arrest and proliferating cell nuclear antigen. Phosphorylated focal adhesion kinase (p-FAK) was also suppressed by EDS. Also active caspase-9, caspase-3 and cleaved poly(ADP-ribose) polymerase (PARP) protein expression levels were increased by administration with EDS; the apoptotic pathway may play an important role in the regulatory effects of EDS on cell growth. These observations provide a mechanism of EDS in attenuating cell proliferation, thus as a potential intervention for restenosis

    ANALGESIC AND ANTI-INFLAMMATORY ACTIVITIES OF AN ETHANOL EXTRACT OF DUNALIELLA SALINA TEOD. (CHLOROPHYCEAE)

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    This study investigated the analgesic and anti-inflammatory effects of an ethanol extract of Dunaliella salina Teod. (Chlorophyceae) (EDS) in Imprinting Control Region mice. Standard all-trans-beta-carotene and the amount of all-trans-beta-carotene in an EDS were analyzed by high-performance liquid chromatography (HPLC). In HPLC analysis, the fingerprint chromatogram of EDS was established. Both all-trans-beta-carotene and EDS showed similar peaks at the retention time of 24 min. This implied that EDS contained the active ingredient all-trans-beta-carotene. Treatment of animals with EDS significantly inhibited the numbers of acetic acid-induced writhing responses at doses of 0.5 g/kg (P < 0.01), 1.0 g/kg (P < 0.001) and 2.0 g/kg (P < 0.001). This inhibitory effect of EDS (1.0 and 2.0 g/kg) on acetic acid-induced writhings was similar to that of the positive control indomethacin (10 mg/kg) (P < 0.001). EDS did not significantly inhibit the formalin-induced pain in the early phase; however, at doses of 0.1 g/kg (P < 0.01), 0.5, 1.0 and 2.0 g/kg, EDS significantly inhibited the formalin-induced pain in the late phase (P < 0.001). Finally, EDS at doses of 1.0 and 2.0 g/kg also inhibited the development of paw edema induced by lambda-carrageenan (carrageenan). EDS (1.0 and 2.0 mg/kg) decreased the level of nitiric oxide (NO) in edematous paw tissue and in serum level, and diminished the level of serum tumor necrosis factor-alpha (TNF-alpha) at the fifth hour after carrageenan injection. Based on these findings, EDS probably exerts anti-inflammatory effects by suppressing TNF-alpha and NO. These results suggest that EDS might be a potential pharmacological analgesic and anti-inflammatory agent. PRACTICAL APPLICATIONS Dunaliella salina (Dunal) Teod. is a valuable beta-carotene source. D. salina is cultivated in a great quantity in the southern part of Taiwan. In order to find its potential application for this product, the analgesic and anti-inflammatory effects were investigated. It was found that D. salina could attenuate the acetic acid-induced writhings and formalin-induced analgesia. We also demonstrate that D. salina could lessen the carrageenan-induced paw edema. Also, the anti-inflammatory effects verified that nitric oxide and TNF-alpha could play an import role

    Analgesic and anti-inflammatory activities of a water extract of Trachelospermum jasminoides (Apocynaceae)

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    Aims of the study: This study investigated the analgesic and anti-inflammatory effects of a water extract of Trachelospermum jasminoides (WET) in ICR mice. Materials and methods: In HPLC analysis, the fingerprint chromatogram of WET was established. Acetic acid-induced writhing response and formalin-induced pain were examined the analgesics effects of WET. WET on X-Carrageenan(carr)-induced paw edema was performed. We investigate the anti-inflammatory mechanism of WET via studies of the activities of glutaithione peroxidase (GPx), glutathione reductase (GRx) in the liver and the levels of malondialdehyde (MDA) and nitrite oxide (NO) in the edema paw. Serum NO and TNF-alpha were also measured. Results: The fingerprint chromatogram of WET was established through HPLC analysis, and implies that WET contains the active ingredient gallic acid, chlorgenic acid, caffeic acid, taxifolin, isoquercitrin and quercetin. WET significantly inhibited the numbers of acetic acid-induced writhing responses and the formalin-induced pain in the late phase. In the anti-inflammatory test, WET inhibited the development of paw edema induced by carr. WET decreased the paw edema at the third, fourth and fifth hour after carr administration, and increased the activities of SOD, GPx and GRx in the liver tissue and decreased the MDA level in the edema paw at the third hour after carr injection. WET decreased the level of NO in edematous paw tissue and in serum level, and diminished the level of serum TNF-alpha at the fifth hour after carr injection. Conclusions: These results demonstrated that WET is an effective anti-inflammatory agent in carr-induced inflammation. WET probably exerts anti-inflammatory effects by suppressing TNF-alpha and NO. The anti-inflammatory mechanism of WET might be related to the decrease in the level of MDA in the edema paw via increasing the activities of SOD, GPx and GRx in the liver. (C) 2009 Elsevier Ireland Ltd. All rights reserved

    Pipoxolan inhibits proliferation of HL-60 human leukaemia cancer cells by arresting the cell cycle at the G(0)/G(1) phase

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    P>1. The aim of the present study was to investigate the molecular mechanisms by which pipoxolan exerts its inhibitory effects and apoptotic activity in human leukaemia HL-60 cells. 2. The effects of pipoxolan on the proliferation of HL-60 cells and on the distribution of cells within different phases of the cell cycle were investigated indirectly using a Trypan blue assay and a flow cytometer, respectively. The effects of pipoxolan on the apoptosis of HL-60 cells was investigated using DNA fragmentation and flow cytometer. The expression of factors affecting the cell cycle and apoptosis, including p53, p21, Bax, Bcl2, cytochrome c, caspase 3 and caspase 9, was examined by western blotting. 3. At 6.25 mu g/mL, pipoxolan significantly induced apoptosis in human leukaemia HL-60 cells after 24 h exposure. In addition, HL-60 cells were arrested in the G(0)/G(1) phase via the induction of p53/p21 by pipoxolan. Apoptosis was associated with an increased Bax/Bcl-2 ratio, cytochrome c release, cleavage of procaspases-9 and -3 and hydrolysis of poly(ADP-ribose) polymerase. Intracellular reactive oxygen species (ROS) seem to play a key role in the pipoxolan-induced apoptosis, because high levels of ROS were produced early in the drug treatment. Apoptosis was significantly abrogated by the free radical scavenger N-acetylcysteine (NAC)
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