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Abstract
In the present investigation, we prepared four different solvent fractions (chloroform, hexane, butanol, and ethyl acetate) of Moringa oleifera extract to evaluate its anti-inflammatory potential and cellular mechanism of action in lipopolysaccharide (LPS)-induced RAW264.7 cells. Cell cytotoxicity assay suggested that the solvent fractions were not cytotoxic to macrophages at concentrations up to 200 µg/mL. The ethyl acetate fraction suppressed LPS-induced production of nitric oxide and proinflammatory cytokines in macrophages in a concentration-dependent manner and was more effective than the other fractions. Immunoblot observations revealed that the ethyl acetate fraction effectively inhibited the expression of inflammatory mediators including cyclooxygenase-2, inducible nitric oxide synthase, and nuclear factor (NF)-κB p65 through suppression of the NF-κB signaling pathway. Furthermore, it upregulated the expression of the inhibitor of κB (IκBα) and blocked the nuclear translocation of NF-κB. These findings indicated that the ethyl acetate fraction of M. oleifera exhibited potent anti-inflammatory activity in LPS-stimulated macrophages via suppression of the NF-κB signaling pathway.
Highlights
Inflammation is a natural immunological response to injuries and infections as a result of harmful stimuli, including microbial pathogens, tissue injury, and immunological cross interactions in the body [1]
All fractions were nontoxic to the cells at lower concentrations; the concentrations of the solvent fractions for further anti-inflammatory mechanistic experiments were set at 50, 100, and 200 μg/mL
We investigated the effects of the ethyl acetate fraction on on the the inflammatory inflammatory mediators mediators inducible nitric nitric oxide oxide synthase synthase (iNOS)
Summary
Inflammation is a natural immunological response to injuries and infections as a result of harmful stimuli, including microbial pathogens, tissue injury, and immunological cross interactions in the body [1]. Numerous inflammatory mediators including proinflammatory cytokines, chemokines, free radicals, and certain enzymes are involved in this. Molecules 2016, 21, 1452 inflammatory process mediated by activated immune cells such as monocytes and macrophages [4]. Various signal transduction pathways are involved in the inflammatory process and contribute to both acute and chronic inflammation. Nuclear factor (NF)-κB is central to inflammatory responses and induces the expression of key inflammatory genes. It facilitates the pathogenesis of various chronic inflammatory diseases and disorders [6]. Downregulation of the NF-κB signaling pathway is one of the major targets to alleviate chronic inflammation and its associated diseases
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