2016
DOI: 10.1016/j.jep.2016.05.044
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Poncirin and its metabolite ponciretin attenuate colitis in mice by inhibiting LPS binding on TLR4 of macrophages and correcting Th17/Treg imbalance

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Cited by 54 publications
(22 citation statements)
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“…In order to better study the mechanisms of severe asthma, we urgently need to build a neutrophil-predominant severe asthma model. While OVA is a classic asthma model allergen, exposure to LPS is also known to lead to an increased risk of asthma-like symptoms [ 17 ] and the onset of asthma exacerbations [ 18 , 19 ]. Meanwhile, the development of allergic asthma is strongly associated with the exposure to HDM [ 20 , 21 ].…”
Section: Discussionmentioning
confidence: 99%
“…In order to better study the mechanisms of severe asthma, we urgently need to build a neutrophil-predominant severe asthma model. While OVA is a classic asthma model allergen, exposure to LPS is also known to lead to an increased risk of asthma-like symptoms [ 17 ] and the onset of asthma exacerbations [ 18 , 19 ]. Meanwhile, the development of allergic asthma is strongly associated with the exposure to HDM [ 20 , 21 ].…”
Section: Discussionmentioning
confidence: 99%
“…Saikosaponin A inhibited LPS induced nuclear factor- κ B (NF- κ B) and interferon regulatory factor 3 (IRF3) activation and the production of tumor necrosis factor- α (TNF- α ), interleukin- (IL-) 1 β , IL-6 and regulated upon activation normal T-cell expressed and secreted (RANTES) in primary mouse macrophages [30]. Poncirin also inhibited the activation of macrophages stimulated with LPS through the inhibition of LPS binding on Toll-like receptor-4 (TLR4) of macrophages [31]. Paeoniflorin exerted anti-inflammatory effects on primary human hepatic sinusoidal endothelial cells through blocking IL-8 secretion via downregulation of extracellular signal-regulated kinase (ERK) 1/2 and Akt phosphorylation [32].…”
Section: Discussionmentioning
confidence: 99%
“…Among the various types of identified phytochemicals in HECA, the therapeutic effects of coumarins (e.g., scopoletin and isoimperatorin), flavonoids (e.g., hesperidin, isoquercetin, miscanthoside, naringin, naringenin, nobiletin, poncirin, quercetin, rutin, tangeritin, vitexin), lignans (e.g., acanthoside D), phenolics (e.g., ferulic acid), and sesquiterpenes (e.g., abscisic acid) have been reported against UC in animal models and human studies [12,17,[24][25][26][27][28][29][30][31][32][33][34]. These phytochemicals inhibited the overproduction of inflammatory mediators (e.g., TNF-α, IL-1β, IL-4, IL-6, IL-17, and continued prostaglandin E 2 ) and oxidative stress (e.g., nitric oxide, myeloperoxidase, superoxide dismutase, and malonaldehyde) while improving colonic structural damage (e.g., occludin, claudin-1, and zona occludens protein-1).…”
Section: Resultsmentioning
confidence: 99%