Moringa oleiferaFlower Extract Suppresses the Activation of Inflammatory Mediators in Lipopolysaccharide-Stimulated RAW 264.7 Macrophages via NF-κB Pathway

Author:

Tan Woan Sean1,Arulselvan Palanisamy1,Karthivashan Govindarajan1,Fakurazi Sharida12

Affiliation:

1. Laboratory of Vaccines and Immunotherapeutics, Institute of Bioscience, Universiti Putra Malaysia, 43400 Serdang, Selangor, Malaysia

2. Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 Serdang, Selangor, Malaysia

Abstract

Aim of Study.Moringa oleiferaLam. (M. oleifera) possess highest concentration of antioxidant bioactive compounds and is anticipated to be used as an alternative medicine for inflammation. In the present study, we investigated the anti-inflammatory activity of 80% hydroethanolic extract ofM. oleiferaflower on proinflammatory mediators and cytokines produced in lipopolysaccharide- (LPS-) induced RAW 264.7 macrophages.Materials and Methods. Cell cytotoxicity was conducted by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Nitric oxide (NO) production was quantified through Griess reaction while proinflammatory cytokines and other key inflammatory markers were assessed through enzyme-linked immunosorbent assay (ELISA) and immunoblotting.Results. Hydroethanolic extract ofM. oleiferaflower significantly suppressed the secretion and expression of NO, prostaglandin E2(PGE2), interleukin- (IL-) 6, IL-1β, tumor necrosis factor-alpha (TNF-α), nuclear factor-kappa B (NF-κB), inducible NO synthase (iNOS), and cyclooxygenase-2 (COX-2). However, it significantly increased the production of IL-10 and IκB-α(inhibitor ofκB) in a concentration dependent manner (100 μg/mL and 200 μg/mL).Conclusion. These results suggest that 80% hydroethanolic extract ofM. oleiferaflower has anti-inflammatory action related to its inhibition of NO, PGE2, proinflammatory cytokines, and inflammatory mediator’s production in LPS-stimulated macrophages through preventing degradation of IκB-αin NF-κB signaling pathway.

Funder

Universiti Putra Malaysia

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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