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    Article

    Luteolin is a bioflavonoid that attenuates adipocyte‑derived inflammatory responses via suppression of nuclear factor‑κB/mitogen‑activated protein kinases pathway

    Sarmila Nepali1★, Ji‑Seon Son1★, Barun Poudel1, Ji‑Hyun Lee1, Young‑Mi Lee3, Dae‑Ki Kim1★★ Corresponding author

    1. 1Department of Immunology and Institute of Medical Sciences, Medical School, Chonbuk National University.
    2. 2Department of Anesthesiology and Pain Medicine, Medical School, Chonbuk National University, Jeonju, Jeonbuk 561‑756.
    3. 3Department of Oriental Pharmacy, College of Pharmacy and Wonkwang‑Oriental Medicines Research Institute, Wonkwang University, Iksan, Jeonbuk, 570‑749, Korea.

    CORRESPONDENCE

    Sarmila Nepali

    Department of Immunology and Institute of Medical Sciences, Medical School, Chonbuk National University.

    daekim@jbnu.ac.kr

    Received: 04-11-2014; Revised: 27-12-2014.

    Volume 11, Issue 43 · pp. 627–635 · PUBLISHED 10 July 2015 · DOI: 10.4103/0973-1296.160470

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Background: Inflammation of adipocytes has been a therapeutic target for treatment of obesity and metabolic disorders which cause insulin resistance and hence lead to type II diabetes. Luteolin is a bioflavonoid with many beneficial properties such as antioxidant, antiproliferative, and anti‑cancer. Objectives: To elucidate the potential anti‑inflammatory response and the underlying mechanism of luteolin in 3T3‑L1 adipocytes. Materials and Methods: We stimulated 3T3‑L1 adipocytes with the mixture of tumor necrosis factor‑α, lipopolysaccharide, and interferon‑γ (TLI) in the presence or absence of luteolin. We performed Griess’ method for nitric oxide (NO) production and measure mRNA and protein expressions by real‑time polymerase chain reaction and western blotting, respectively. Results: Luteolin opposed the stimulation of inducible nitric oxide synthase and NO production by simultaneous treatment of adipocytes with TLI. Furthermore, it reduced the pro‑inflammatory genes such as cyclooxygenase‑2, interleukin‑6, resistin, and monocyte chemoattractant protein‑1. Furthermore, luteolin improved the insulin sensitivity by enhancing the expression of insulin receptor substrates (IRS1/2) and glucose transporter‑4 via phosphatidylinositol‑3K signaling pathway. This inhibition was associated with suppression of IκB‑α degradation and subsequent inhibition of nuclear factor‑κB (NF‑κB) p65 translocation to the nucleus. In addition, luteolin blocked the phosphorylation of ERK1/2, c‑Jun N‑terminal Kinases and also p38 mitogen‑activated protein kinases (MAPKs). Conclusions: These results illustrate that luteolin attenuates inflammatory responses in the adipocytes through suppression of NF‑κB and MAPKs activation, and also improves insulin sensitivity in 3T3‑L1 cells, suggesting that luteolin may represent a therapeutic agent to prevent obesity‑associated inflammation and insulin resistance.

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      Nepali, S., Son, J., Poudel, B., Lee, J., Lee, Y., & Kim, D. (2015). Luteolin is a bioflavonoid that attenuates adipocyte‑derived inflammatory responses via suppression of nuclear factor‑κB/mitogen‑activated protein kinases pathway. Pharmacognosy Magazine, 11(43), 627–635. https://doi.org/10.4103/0973-1296.160470