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 Iκ-B-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.