ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2014
Nuclear factor-κB activation inhibitor attenuates ischemia reperfusion injury and inhibits Hmgb1 expression.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Ischemic postconditioning ameliorates acute kidney injury induced by limb ischemia/reperfusion via transforming TLR4 and NF-κB signaling in rats.Journal of orthopaedic surgery and research · 2021Article
- Downregulation of lncRNA ZFAS1 protects H9c2 cardiomyocytes from ischemia/reperfusion‑induced apoptosis via the miR‑590‑3p/NF‑κB signaling pathway.Molecular medicine reports · 2020Article
- Hsp27 reduces cold ischemia-reperfusion injury in heart transplantation through regulation of NF-κB and PUMA signaling.International journal of clinical and experimental pathology · 2018Article
- HMGB1, TGF-β and NF-κB are associated with chronic allograft nephropathy.Experimental and therapeutic medicine · 2017Article
- [Protective effect of exosome on organs after ischemia-reperfusion injury].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2017Review
- Inhibition of PKR protects against HScientific reports · 2016Article
- Simulated ischemia/reperfusion-induced p65-Beclin 1-dependent autophagic cell death in human umbilical vein endothelial cells.Scientific reports · 2016Article
- TLR4-HMGB1-, MyD88- and TRIF-dependent signaling in mouse intestinal ischemia/reperfusion injury.World journal of gastroenterology · 2015Article
- Soluble Receptor for Advanced Glycation End Product Ameliorates Chronic Intermittent Hypoxia Induced Renal Injury, Inflammation, and Apoptosis via P38/JNK Signaling Pathways.Oxidative medicine and cellular longevityArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
OBJECTIVE AND
designTo investigate the effects of nuclear factor-κB activation inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) on cardiac ischemia reperfusion injury in a transplantation model.
methodsHearts of C57BL/6 mice were flushed and stored in cold Bretschneider solution for 8 h and then transplanted into syngeneic recipient. Some mice were administrated intraperitoneally with DHMEQ (8 mg/kg) 1 h before reperfusion. For inhibition of Hmgb1, mice were treated with glycyrrhizin at 250 mg/kg prior to reperfusion.
resultsDHMEQ decreased cardiomyocyte apoptosis and recruitment of neutrophils and macrophages. Troponin T (TnT) production on 24 h after myocardial IR injury was reduced by DHMEQ treatment. Cardiac output at 60 mmHg of afterload pressure was significantly increased in hearts with DHMEQ treatment (IR+DHMEQ: 58.6 ± 5.75 ml/min; IR: 25.9 ± 4.1 ml/min; P < 0.05). Furthermore, DHMEQ suppressed high mobility group protein (Hmgb1) expression. And the Caspase 3 activity, the number of TUNEL-positive cardiomyocytes and infiltrated neutrophil in cardiac allograft were markedly decreased with Hmgb1 inhibitor treatment.
conclusionsNuclear factor-κB activation inhibitor DHMEQ attenuates ischemia reperfusion injury in a cardiac transplantation model and it may be a suitable agent for the protection of the cardiac against ischemia reperfusion injury.
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