2017
DOI: 10.1016/j.biopha.2017.07.041
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Subcritical water-hydrolyzed fish collagen ameliorates survival of endotoxemic mice by inhibiting HMGB1 release in a HO-1-dependent manner

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Cited by 11 publications
(3 citation statements)
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“…NO accumulated in culture medium was determined by measuring the levels of nitrite (an oxidized form of NO) as described previously (Ahn, Hwang, Ham, et al., 2017). Briefly, 100‐μl aliquot of conditioned culture medium was mixed with 100 μl of Griess reagent (equal part of 0.1% N‐(1‐naphthyl)‐ethylenediamine dihydrochloride and 1% sulfanilamide) and incubated for 10 min at room temperature.…”
Section: Methodsmentioning
confidence: 99%
See 1 more Smart Citation
“…NO accumulated in culture medium was determined by measuring the levels of nitrite (an oxidized form of NO) as described previously (Ahn, Hwang, Ham, et al., 2017). Briefly, 100‐μl aliquot of conditioned culture medium was mixed with 100 μl of Griess reagent (equal part of 0.1% N‐(1‐naphthyl)‐ethylenediamine dihydrochloride and 1% sulfanilamide) and incubated for 10 min at room temperature.…”
Section: Methodsmentioning
confidence: 99%
“…Furthermore, formononetin, a herbal isoflavonoid, inhibited LPS‐triggered release of HMGB1 by upregulating SIRT1 (sirtuin 1; silent mating type information regulation 2 homologue 1) in a peroxisome proliferator‐activated receptor (PPAR)δ‐dependent manner (Hwang et al., 2018). In addition, fish collagen hydrolyzed by subcritical water also improved the survival of endotoxemic mice by transcriptional induction of heme oxygenase‐1 (HO‐1) in a nuclear factor erythroid 2‐related factor 2 (Nrf 2) signaling, thereby inhibiting HMGB1 secretion into the circulation (Ahn, Hwang, Ham, et al., 2017). In particular, JAK/STAT1 (Janus kinase/signal transducer and activator of transcription 1) signaling plays a pivotal role in the HMGB1 translocation from nucleus to cytoplasm through promotion of HMGB1 hyperacetylation in LPS‐treated cells (Lu et al., 2014).…”
Section: Introductionmentioning
confidence: 99%
“…M2 macrophages produce anti-inflammatory mediators such as heme oxygenase-1 (HO-1) and NADPH dehydrogenase quinone 1 (NQO1). HO-1, which maintains cellular redox homeostasis, is expressed at a low levels in unstimulated normal cells [8,9]. However, HO-1 expression is increased by lipopolysaccharides (LPS), oxidative stress, pro-inflammatory cytokines, and transforming growth factor-β1 (TGF-β1) and protects cells from oxidative stress and inflammation [10,11].…”
Section: Introductionmentioning
confidence: 99%