Abstract

Cocoa is a rich source of polyphenols that has been traditionally used as the treatment of several types of inflammation related disease. The response to inflammation comprises the consecutive release of mediators and the enlistment of circulating leukocytes, such as macrophages. Currently, Cocoa-derived polyphenolics have shown anti-inflammatory effects in vivo, but the therapeutic benefits in vitro remain unclear. Therefore, in this study, the effect of cocoa polyphenolic extract (CPE) on RAW 264.7 macrophage cells sensitized by lipopolysaccharide as in vitro inflammatory model was investigated. The anti-inflammatory activity of CPE was assessed by measuring its ability to inhibit the pro-inflammatory enzyme 5-lipoxygenase (5-LOX) and the pro-inflammatory mediators prostaglandin E2 (PGE2), reactive oxygen species (ROS), nitric oxide (NO) and tumor necrosis factor-alpha (TNF-α). The results show that CPE significantly inhibits 5-LOX activity (p < 0.01). In addition, CPE dose-dependently suppressed the production of PGE2, ROS, NO and TNF-α in RAW 264.7 cells. These data suggest that CPE may be used for the treatment of inflammation and it’s related-diseases.

Highlights

  • Reactive oxygen species (ROS) are naturally and continuously produced as a result of cellular metabolism in all aerobic organisms

  • The response to inflammation comprises the consecutive release of mediators and the enlistment of circulating leukocytes, such as macrophages, that become stimulated at the area of inflammation, thereby releasing various types of mediators and cytokines with either pro- or anti-inflammatory actions, such as IL-1β, IL-6, nitric oxide (NO), tumor necrosis factor-alpha (TNF-α) and PG (Day 2002; Feldmann et al 1996)

  • Inhibitory effect of cocoa polyphenolic extract (CPE) on ROS formation To investigate whether CPE can inhibit intracellular ROS, RAW 264.7 macrophage cells were treated with varying concentrations of CPE and exposed to H2O2

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Summary

Introduction

Reactive oxygen species (ROS) are naturally and continuously produced as a result of cellular metabolism in all aerobic organisms. Respiratory bursts produced by inflammatory cells lead to the increased production and accumulation of ROS at the site of damage (Hussain et al 2003). The response to inflammation comprises the consecutive release of mediators and the enlistment of circulating leukocytes, such as macrophages, that become stimulated at the area of inflammation, thereby releasing various types of mediators and cytokines with either pro- or anti-inflammatory actions, such as IL-1β, IL-6, NO, TNF-α and PG (Day 2002; Feldmann et al 1996). These inflammatory mediators have either pro- or anti- inflammatory actions (Bessis and Boissier 2001). Excessive leakage and stimulation of cells induce tissue damage, resulting in pain and edema

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