Trigonelline Attenuates Lipopolysaccharide-Induced Nitric Oxide Production and Downregulates Inflammation Associated Gene Expressions

Abstract

　Trigonelline, an N-methylnicotinic acid, is found in fenugreek (Trigonella foenum-graecum L.) and coffee beans. Trigonelline has been reported to prevent cardiovascular and Alzheimer's diseases. However, the potential pharmacological application of trigonelline in in fl ammatory responses is poorly understood, particularly in macrophages. In the present study, we investigated the effects and underlying molecular mechanisms of trigonelline on 100ng/mℓ lipopolysaccharide (LPS) -induced inflammatory responses in RAW264.7 mouse macrophages. 50μM Trigonelline elicited a marked reduction in LPS-mediated production of nitric oxide (NO) compared with LPS-treated cells. Subsequently, the mRNA expression levels of inducible nitric oxide (iNOS), cyclooxygenase-2 (COX2), and pro-inflammatory cytokines, including tumor necrosis factor α (TNF-α), interleukin (IL) -6, and IL-1β in LPS-treated cells were significantly decreased by trigonelline co-treatment. Furthermore, we found that treatment of cells with LPS elevated the gene expression of reactive oxidative species (ROS) -associated molecules, such as p47^phox and p67^phox, whereas trigonelline treatment significantly decreased them. Our data suggested that trigonelline inhibited inflammation and oxidative stress, resulting in the potential application of this compound in the prevention of infl ammatory diseases.