Abstract

Vernonia amygdalina (VA) has been reported to have antioxidant potential; however, its DNA protection and anti-inflammatory properties remain unclear. We aimed to investigate whether aqueous (WEVAL) and alcoholic (EEVAL) VA extracts exert similar antioxidant, DNA protection and anti-inflammatory effects and attempted to explore the mechanism underlying the anti-inflammatory effects. These results demonstrated that WEVAL had greater polyphenolic and flavonoid contents, as well as a stronger reducing power, DPPH radical scavenging and DNA protective activity. Moreover, both extracts reduced lipopolysaccharide (LPS)-induced expression of COX-II, iNOS, pro-inflammatory factors, including NO, TNF-α, IL-1β, and IL-10. Compared with WEVAL, EEVAL was a more potent inflammatory inhibitor. Both extracts similarly inhibited LPS-induced MAPK (p38) and NF-κB expression. Our findings indicate that WEVAL and EEVAL have diverse antioxidant and anti-inflammatory effects. WEVAL had a stronger antioxidant and DNA protection activity; contrastingly, EEVAL had a stronger anti-inflammatory ability. The anti-inflammatory activity involves reduced pro-inflammatory cytokines through NF-κB down-regulation and MAPK inhibition. These results demonstrated that production of WEVAL and EEVAL from VA leaves may provide a safe and efficacious source of pharmaceutical applications, with antioxidant, DNA protective and anti-inflammation activities.

Highlights

  • Inflammation is a self-protective body mechanism for the prevention and removal of harmful stimuli

  • We aimed to investigate the effects of WEVAL and EEVAL on antioxidant, DNA protection and LPS-induced inflammation and to determine the underlying biochemical mechanism

  • We evaluated the effects of the Vernonia amygdalina (VA) leaf extracts on the gene expression of iNOs and NO production and found that both WEVAL and EEVAL showed dose-dependent inhibition of LPS-induced NO production in RAW 264.7 macrophage cells (Fig 3(A) and 3(B)) with inducible NOs production showing a similar trend (Fig 3(C) and 3(D))

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Summary

Introduction

Inflammation is a self-protective body mechanism for the prevention and removal of harmful stimuli. Especially macrophages, play an important role in the inflammation process. Through lipopolysaccharide (LPS) stimulation, macrophages initiate intracellular signal cascades for the synthesis of the pro-inflammatory cytokine, e.g., IL-1, IL-6, and TNF-α [1]. The most important intracellular signaling proteins for inflammation are NF-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs).

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