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      Anti‐inflammatory and anti‐insulin resistance activities of aqueous extract from Anoectochilus burmannicus

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          Abstract

          This study investigated biological activities including antioxidative stress, anti‐inflammation, and anti‐insulin resistance of Anoectochilus burmannicus aqueous extract ( ABE). The results showed abilities of ABE to scavenging DPPH and ABTS free radicals in a dose‐dependent manner. Besides, ABE significantly reduced nitric oxide ( NO) production in the lipopolysaccharide ( LPS)‐treated RAW 264.7 via inhibition of mRNA and protein expressions of nitric oxide synthase ( iNOS). The LPS‐induced mRNA expressions of cyclooxygenase‐2 ( COX‐2) and interleukin 1β ( IL‐1β) were suppressed by ABE. Moreover, ABE exerted anti‐insulin resistance activity as it significantly improved the glucose uptake in tumor necrosis factor ( TNF)‐α treated 3T3‐L1 adipocytes. In addition, ABE at the concentration of up to 200 μg/ mL was not toxic to human peripheral blood mononuclear cells ( PBMCs) and did not induce mutations. Finally, the results of our study suggest the potential use of A. burmannicus as anti‐inflammatory, anti‐insulin resistance agents, or food supplement for prevention of chronic diseases.

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          Most cited references58

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          Role of nitric oxide in inflammatory diseases.

          Nitric oxide (NO) is a signaling molecule that plays a key role in the pathogenesis of inflammation. It gives an anti-inflammatory effect under normal physiological conditions. On the other hand, NO is considered as a pro-inflammatory mediator that induces inflammation due to over production in abnormal situations. NO is synthesized and released into the endothelial cells by the help of NOSs that convert arginine into citrulline producing NO in the process. Oxygen and NADPH are necessary co-factors in such conversion. NO is believed to induce vasodilatation in cardiovascular system and furthermore, it involves in immune responses by cytokine-activated macrophages, which release NO in high concentrations. In addition, NO is a potent neurotransmitter at the neuron synapses and contributes to the regulation of apoptosis. NO is involved in the pathogenesis of inflammatory disorders of the joint, gut and lungs. Therefore, NO inhibitors represent important therapeutic advance in the management of inflammatory diseases. Selective NO biosynthesis inhibitors and synthetic arginine analogues are proved to be used for the treatment of NO-induced inflammation. Finally, the undesired effects of NO are due to its impaired production, including in short: vasoconstriction, inflammation and tissue damage.
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            Anti-Inflammatory Effects of Flavonoids: Genistein, Kaempferol, Quercetin, and Daidzein Inhibit STAT-1 and NF-κB Activations, Whereas Flavone, Isorhamnetin, Naringenin, and Pelargonidin Inhibit only NF-κB Activation along with Their Inhibitory Effect on iNOS Expression and NO Production in Activated Macrophages

            In inflammation, bacterial products and proinflammatory cytokines induce the formation of large amounts of nitric oxide (NO) by inducible nitric oxide synthase (iNOS), and compounds that inhibit NO production have anti-inflammatory effects. In the present study, we systematically investigated the effects of 36 naturally occurring flavonoids and related compounds on NO production in macrophages exposed to an inflammatory stimulus (lipopolysaccharide, LPS), and evaluated the mechanisms of action of the effective compounds. Flavone, the isoflavones daidzein and genistein, the flavonols isorhamnetin, kaempferol and quercetin, the flavanone naringenin, and the anthocyanin pelargonidin inhibited iNOS protein and mRNA expression and also NO production in a dose-dependent manner. All eight active compounds inhibited the activation of nuclear factor- κ B (NF- κ B), which is a significant transcription factor for iNOS. Genistein, kaempferol, quercetin, and daidzein also inhibited the activation of the signal transducer and activator of transcription 1 (STAT-1), another important transcription factor for iNOS. The present study characterises the effects and mechanisms of naturally occurring phenolic compounds on iNOS expression and NO production in activated macrophages. The results partially explain the pharmacological efficacy of flavonoids as anti-inflammatory compounds.
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              Ferulic Acid: Therapeutic Potential Through Its Antioxidant Property

              There has been considerable public and scientific interest in the use of phytochemicals derived from dietary components to combat human diseases. They are naturally occurring substances found in plants. Ferulic acid (FA) is a phytochemical commonly found in fruits and vegetables such as tomatoes, sweet corn and rice bran. It arises from metabolism of phenylalanine and tyrosine by Shikimate pathway in plants. It exhibits a wide range of therapeutic effects against various diseases like cancer, diabetes, cardiovascular and neurodegenerative. A wide spectrum of beneficial activity for human health has been advocated for this phenolic compound, at least in part, because of its strong antioxidant activity. FA, a phenolic compound is a strong membrane antioxidant and known to positively affect human health. FA is an effective scavenger of free radicals and it has been approved in certain countries as food additive to prevent lipid peroxidation. It effectively scavenges superoxide anion radical and inhibits the lipid peroxidation. It possesses antioxidant property by virtue of its phenolic hydroxyl group in its structure. The hydroxy and phenoxy groups of FA donate electrons to quench the free radicals. The phenolic radical in turn forms a quinone methide intermediate, which is excreted via the bile. The past few decades have been devoted to intense research on antioxidant property of FA. So, the present review deals with the mechanism of antioxidant property of FA and its possible role in therapeutic usage against various diseases.
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                Author and article information

                Contributors
                arisa.bonness@cmu.ac.th
                Journal
                Food Sci Nutr
                Food Sci Nutr
                10.1002/(ISSN)2048-7177
                FSN3
                Food Science & Nutrition
                John Wiley and Sons Inc. (Hoboken )
                2048-7177
                26 August 2016
                May 2017
                : 5
                : 3 ( doiID: 10.1002/fsn3.2017.5.issue-3 )
                : 486-496
                Affiliations
                [ 1 ] Department of Biochemistry Faculty of MedicineChiang Mai University Meung Chiang MaiThailand
                [ 2 ] Food and Nutritional Toxicology Unit Institute of NutritionMahidol University Salaya Nakhon PathomThailand
                Author notes
                [*] [* ] Correspondence

                Arisa Imsumran, Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.

                Email : arisa.bonness@ 123456cmu.ac.th

                Article
                FSN3416
                10.1002/fsn3.416
                5449198
                28572933
                83a67b9e-a565-4b90-b279-0ff10f2cdf73
                © 2016 The Authors. Food Science & Nutrition published by Wiley Periodicals, Inc.

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 23 May 2016
                : 18 July 2016
                : 31 July 2016
                Page count
                Figures: 4, Tables: 1, Pages: 11, Words: 7939
                Funding
                Funded by: Plant Genetic Conservation Project under the Royal Initiative of Her Royal Highness Princess Maha Chakri Sirindhorn, Thailand
                Funded by: The National Research Council of Thailand (NRCT)
                Funded by: Faculty of Medicine Research Fund, Chiang Mai University, Chiang Mai, Thailand
                Categories
                Original Research
                Original Research
                Custom metadata
                2.0
                fsn3416
                May 2017
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.0.9 mode:remove_FC converted:30.05.2017

                3t3‐l1 adipocyte,anoectochilus burmannicus,inflammation,insulin resistance,raw264.7 macrophage

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