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        Anti-inflammatory Activities of Lupane-triterpenoids In Vitro and Their Phytochemical Fingerprinting from Leaves of Acanthopanax gracilistylus

        Xiao Jun Li,Ling Dai,Zhi Li,Xiao Dan Zhang,Xiang Qian Liu,Qin Peng Zou,Xia Xie 한국생약학회 2015 Natural Product Sciences Vol.21 No.2

        The activities on the inhibition of NO on LPS-induced RAW 264.7 macrophages were investigated in this work. A simple and sensitive method has been developed and validated for fingerprinting analysis of leaves of Acanthopanax gracilistylus W.W. Smith (AGS). The cytotoxicity and inhibition of NO on LPS-induced RAW 264.7 cells of the extract and triterpenoids were determined. Optimal conditions of HPLC analysis were established as follows. The separation was performed with an ODS-C18 column at 30 oC, the detected wavelength was 210 nm, the flow rate was 1 mL/min, and the mobile phase consisted of acetonitrile (0.05% phosphoric acid) -0.05% phosphoric acid solution with gradient elution. Our results showed that impressic acid and acankoreaogenin was more effective on the inhibition of NO than the methanol extract and other compounds. There were seventeen peaks coexisted with similarities above 0.95 and nine lupane-triterpenoids including acankoreaogenin and impressic acid detected and identified. The result of anti-inflammatory activities provides a potential explanation for the use of AGS leaves as a herbal medicine in the treatment of inflammatory diseases. Our results also show that acankoreanogenin and impressic acid may be potentially useful in developing new anti-inflammatory agents. In addition, the fingerprint chromatography clearly illustrated and confirmed the material basis for the anti-inflammatory activities of this plant.

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        Myricetin Protects Against Cytokine-Induced Cell Death in RIN-m5f β Cells

        Ye Ding,Zhao-Feng Zhang,Xiao-Qian Dai,Yong Li 한국식품영양과학회 2012 Journal of medicinal food Vol.15 No.8

        Cytokine-induced cell death is recognized as a major cause of progressive β-cell loss. Tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and interferon γ (IFN-γ) in combination trigger a series of events that lead to β-cell death. In the past few decades, the use of myricetin as an anti-inflammatory and cytoprotective agent has gained much attention. The present study focused on the protective roles of myricetin against cytokine-induced cell death in insulin-secreting RIN-m5f β cells. The results showed that myricetin (especially at concentrations of 10 μM and 20 μM) increased cell viability and decreased cell apoptosis induced by the cytokine mixture of TNF-α (10 ng/mL), IL-1β (5 ng/mL), and IFN-γ (1000 IU/mL) for 3 days. Moreover, the cytokines increased the total and p65 subunit levels of nuclear factor κB, decreased inhibitor κB α levels, stimulated the accumulation of nitric oxide, increased cytochrome c release from mitochondria, and induced reactive oxygen species generation; myricetin (especially at the concentration of 20 μM) abolished all of these parameters. These results suggest that myricetin might have therapeutic value for preventing β-cell death.

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