Abstract
We investigated whether isoleucilactucin, an active constituent of Ixeridium dentatum, reduces inflammation caused by coal fly ash (CFA) in alveolar macrophages (MH-S). The anti-inflammatory effects of isoleucilactucin were assessed by measuring the concentration of nitric oxide (NO) and the expression of pro-inflammatory mediators in MH-S cells exposed to CFA-induced inflammation. We found that isoleucilactucin reduced CFA-induced NO generation dose-dependently in MH-S cells. Moreover, isoleucilactucin suppressed CFA-activated proinflammatory mediators, including cyclooxygenase-2 (COX2) and inducible NO synthase (iNOS), and the proinflammatory cytokines such as interleukin-(IL)-1β, IL-6, and tumor necrosis factor (TNF-α). The inhibiting properties of isoleucilactucin on the nuclear translocation of phosphorylated nuclear factor-kappa B (p-NF-κB) were observed. The effects of isoleucilactucin on the NF-κB and mitogen-activated protein kinase (MAPK) pathways were also measured in CFA-stimulated MH-S cells. These results indicate that isoleucilactucin suppressed CFA-stimulated inflammation in MH-S cells by inhibiting the NF-κB and MAPK pathways, which suggest it might exert anti-inflammatory properties in the lung.
Highlights
Inflammation is a critical aspect of the immune response against cell damage and pathogens, which provides a defense mechanism to remove harmful stimuli [1,2,3]
Macrophages play a crucial role in inflammatory processes, primarily by producing proinflammatory mediators that include nitric oxide (NO), inducible NO synthase, cyclooxygenase-2 (COX-2), as well as the cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) [6,7]
Our study showed that isoleucilactucin has anti-inflammatory activities in CFAinduced MH-S cells
Summary
Inflammation is a critical aspect of the immune response against cell damage and pathogens, which provides a defense mechanism to remove harmful stimuli [1,2,3]. Increased movement of plasma and leukocytes from the blood into wounded regions causes acute inflammation, which is an initial response of the organism to damaging stimuli When it becomes chronic, inflammation causes a gradual shift in the cell types present at the site of inflammation and can result in a destruction or regeneration of tissues, depending on the context [4]. -(PAC)RRaTn-PaClyRsisanwaalysspiserwfoarsmpeedrftoormeveadlutaoteevthaelumatRe NthAe lmevReNlsAoflepvreolisnoflfapmrominatfolarmy mmeadtoiarytomrse, dsuiacthorass, scuycclhoaosxycygcelnoaosxey2ge(CnOasXe22)(aCnOdXin2d) auncdibilnednuitcriibcloexniditericsyonxtihdaessey(niNthOasSe),(aiNs wOSel)l, as wpreolilnaflsapmrominaftloarmymcyattookryinceyst,oskuicnhesa,sstuucmh oars ntuemcrorsinsefcarcotosirs-afalpcthoar-(aTlNphFa-α(T),NinFt-eαr)le, uinktienrl(eIuLk)-i6n,(IILL-)1-β6,,IaLn-d1βG, aAnPdDGHA. Isoleucilactucin Ameliorated CFA-Induced mRNA Expression of Proinflammatory Cytokines in MH-S Cells. Following isoleucilactucin (12.5, 25, 50, and 100 μM) administration, the mRNA expression levels of the proinflammatory mediators were markedly and dose-dependently inhibited (Figure 3A–E). Following isoleucilactucin (12.5, 25, 50, and 100 μM) administration, the mRNA expression levels of the proinflammatory mediators 4woef r1e2 markedly and dose-dependently inhibited (Figure 3A–E).
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