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Year : 2015  |  Volume : 11  |  Issue : 43  |  Page : 627-635

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

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

Correspondence Address:
Dae-Ki Kim
Department of Immunology and Institute of Medical Sciences, Medical School, Chonbuk National University, Jeonju, Jeonbuk 561-756
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Source of Support: Ministry of Knowledge Economy (MKE), Korea Institute for Advancement of Technology (KIAT) through the inter-ER Cooperation Projects (R0002019)., Conflict of Interest: None declared.

DOI: 10.4103/0973-1296.160470

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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 a, lipopolysaccharide, and interferon g (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 IkB a 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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