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Abstract
Sanguisorbae Radix (SR) is the root of the Sanguisorba officinalis L., a plant native to Asian countries and used in traditional medicine. We isolated the active components of SR and investigated their anti-inflammatory potential. Quercetin (QC), (+)-catechin (CC), and gallic acid (GA) were isolated from acetone extracts of SR. To elucidate the molecular mechanism by which these compounds suppress inflammation, we analyzed the transcriptional up-regulation of inflammatory mediators, such as nuclear factor-kappa B (NF-κB) and its target genes, inducible NOS (iNOS), and cyclooxygenase (COX)-2, in lipopolysaccharide (LPS)-stimulated macrophage RAW264.7 cells. Notably, QC, CC, and GA were found to inhibit the production of nitric oxide, tumor necrosis factor-alpha, and prostaglandin in a dose-dependent manner. Western blot results indicate that the compounds decreased the expression of iNOS and COX-2 proteins. Furthermore, the compounds decreased phosphorylation of IKK, IκB, ERK, p-38, and JNK proteins in LPS-induced cells. The results support the notion that QC, CC, and GA can potently inhibit the inflammatory response, with QC showing the highest anti-inflammatory activity. In in vivo toxicity studies in zebrafish (Danio rerio), QC showed no toxicity up to 25 μg/mL. Therefore, QC has non-toxic potential as a skin anti-inflammatory biomaterial.
Highlights
Inflammation is a response to injury caused by harmful physical or chemical stimuli or microbiological toxins, and occurs in numerous pathologies, such as asthma, arthritis, multiple sclerosis, atherosclerosis, and inflammatory bowel diseases [1,2]
QC, CC, and gallic acid (GA) were found to inhibit the production of nitric oxide, tumor necrosis factor-alpha, and prostaglandin in a dose-dependent manner
A previous study reported that LPS increased activation of NF-κB and regulated the binds to inhibitory κBα (IκBα) molecules in the promoter region of an inflammatory response and only expression of inducible nitric oxide synthase (NOS) (iNOS), COX-2, and other cytokines [30]; NF-κB plays an important role in becomes active after IκBα is phosphorylated and subsequently degraded; this modification of IκBα inflammation
Summary
Inflammation is a response to injury caused by harmful physical or chemical stimuli or microbiological toxins, and occurs in numerous pathologies, such as asthma, arthritis, multiple sclerosis, atherosclerosis, and inflammatory bowel diseases [1,2]. Lipopolysaccharide (LPS)-induced gene products include pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF)-α and interleukin-6 (IL-6), and adhesion enzymes, such as iNOS and cyclooxygenase-2 (COX)-2 [7]. COX enzymes are known to produce prostaglandins (PGs) that are involved in many physiological events, such as the progression of inflammation, modulation of the inflammatory response, and transmission of pain [8]. COX-2 is only expressed in some tissues and is transiently induced by growth factors, pro-inflammatory cytokines, tumor promoters, and bacterial toxins [9]. Is a DNA transcription factor that plays a vital role in the expression of various genes involved in the inflammatory response [10,11,12]. One of the main functions of MAPK is the activation of transcription factors, some of which increase the expression of pro-inflammatory cytokines [17]. We used the zebrafish (Danio rerio) embryo model to investigate the potential anti-inflammatory mechanism of SR against LPS-induced inflammatory response in macrophages, to evaluate the root as a potential safe cosmetic material
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