Abstract

Acute inflammation is essential for defending the body against pathogens; however, when inflammation becomes chronic, it is harmful to the body and is part of the pathophysiology of various diseases such as Diabetes Mellitus type 2 (DM2) and Cardiovascular Disease (CVD) among others. In chronic inflammation macrophages play an important role, mainly through the secretion of proinflammatory cytokines such as Tumor necrosis factor (TNF)-α and Interleukin (IL)-1β, explained in part by activation of the Toll-like receptor 4 (TLR4), a signaling pathway which culminates in the activation of Nuclear factor (NF)-κB, an important transcription factor in the expression of these proinflammatory genes. On the other hand, the benefits on health of a diet rich in fruit and vegetables are well described. In this work, the effects of aqueous extract of tomato and ferulic acid on the expression of proinflammatory cytokines in LPS activated monocyte-derived THP-1 macrophages were investigated. In addition, using Western blot, we investigated whether the inhibition was due to the interference on activation of NF-κB. We found that both the tomato extract and ferulic acid presented inhibitory activity on the expression of TNF-α and IL-1β cytokine by inhibiting the activation of NF-κB. The current results suggest that tomatoes and ferulic acid may contribute to prevention of chronic inflammatory diseases.

Highlights

  • Acute inflammation is the first response of the organism to control an insulting agent [1]

  • We evaluated the effect of tomato extract and ferulic acid on the expression of proinflammatory cytokines Tumor necrosis factor (TNF)-α and IL-1β and its impact on the activation of Nuclear factor (NF)-κB in LPS-activated macrophages

  • No significant differences between viability of cells incubated with tomato extract or ferulic acid, activated and inactivated, and the macrophages without aqueous tomato extract neither ferulic acid

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Summary

Introduction

Acute inflammation is the first response of the organism to control an insulting agent [1]. Macrophages are major players at the beginning of this process because they recognize microorganisms and dead cells, and produce various proinflammatory mediators such as Interleukin (IL)-1, TNF-α, Interleukin (IL)-6, Prostaglandin E2 (PGE2) and NO [2] These mediators activate endothelial cells and allow the arrival of more cells such as monocytes and neutrophils that fight the pathogen and release more inflammatory mediators [3,4,5]. Lipopolysaccharide (LPS) is recognized by TLR4 and activates a signaling pathway independent or Myeloid differentiation primary response gene 88 (MyD88)-dependent leading to the activation of NF-κB and proinflammatory cytokine production. This signaling pathway is finely regulated to avoid damage to the organism induced by inflammation [9]. Chronic inflammation is a maladapatative process, involved in the pathophysiology of obesity, insulin resistance, DM2 and CVD [10,11]

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