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Abstract
Glasswort (Salicornia herbacea L.) is a halophyte that exhibits antioxidant and antidiabetic effects. Only a few studies have been conducted on its antioxidant effects. Here, we isolated an antioxidant using an activity-based purification method, and the resulting compound was identified as (9Z,11E)-13-Oxooctadeca-9,11-dienoic acid (13-KODE). We investigated its ability to suppress inflammatory responses and the molecular mechanisms underlying these abilities using lipopolysaccharide-stimulated RAW 264.7 macrophage cells. We studied the anti-inflammatory effects of 13-KODE derived from S. herbacea L on RAW 264.7 macrophages. 13-KODE inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) production by suppressing inducible NO synthase and suppressed LPS-induced tumor necrosis factor and interleukin-1β expression in RAW 264.7 macrophages. LPS-mediated nuclear localization of NF-κB and mitogen-activated protein kinase activation were inhibited by 13-KODE. 13-KODE significantly reduced LPS-induced production of reactive oxygen species and increased the expression of nuclear factor erythroid-2 like 2 (Nfe2I2) and heme oxygenase 1. Overall, our results indicate that 13-KODE may have potential for treating inflammation.
Highlights
Inflammation is the complex biological response of body tissues against pathogens and damaged cells [1]
The ground powder of S. herbacea L. was extracted with 100% methanol, and the dried samples of S. herbacea L. were extracted with ethyl acetate acetate (EA) and H2 O (v/v = 1:1)
We found that LPS stimulation increased the nuclear level trol cells, whereas 13-KODE reduced the levels of nuclear p65 by 67% compared of NF-κB p65 protein and down-regulated the expression of IκB-α
Summary
Inflammation is the complex biological response of body tissues against pathogens and damaged cells [1]. It is a protective response involving immune cells and molecular mediators. The function of inflammation is to eliminate necrotic cells and damaged tissues. Infectious agents and cell damage activate inflammatory cells and induce inflammatory signaling pathways, such as NF-κB, mitogen-activated protein kinase (MAPK), and JAKSTAT signaling pathways [3]. Lipopolysaccharide (LPS), an endotoxin derived from the outer membrane of Escherichia coli, induces inflammation and is used to develop disease models to examine the anti-inflammatory effects of drugs and natural compounds [4,5]
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