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google, scholar, article, pubmed, coronary, cas, myocardial, microembolization, heart, heusch, rats, activation, cardiol, basic, nuclear, erbel, schulz, physiol, function, inflammatory, dysfunction, cme, patients, acute, infarction, res, circulation, nfκb, pyrrolidine, dithiocarbamate, ventricular, induced, cardiac, access, factor, privacy, cookies, content, research, cardiology, pdtc, left, cell, injury, regulation, mol, atorvastatin, percutaneous, skyschally, role,

Topics {✒️}

tumor necrosis factor-α lipopolysaccharide-free c-reactive protein month download article/chapter multi-focal myocardial necrosis pyrrolidine dithiocarbamate prevents acute anti-inflammatory treatment xudong sun & lianglong chen peri-procedural myocardial injury nuclear factor-kappab activation c-reactive protein evidence secondary antioxidant-responsive factor dose-dependency significantly suppressed proline-rich membrane anchor nf-κb/dna-binding percent micro-necrotic area percent micro-fibrotic area ischaemia–reperfusion microvascular damage q-wave myocardial infarction armyda-acs randomized trial myocardial reperfusion injury nuclear factor-kappab signaling pathway acute coronary syndromes transcription factor nf-kappa article basic research nuclear factor-κb sprague–dawley rats served perfusion–contraction mismatch secondary related subjects myocardial ischaemia–reperfusion cytokin gene regulation nuclear factor-kappa nuclear factor kappa full article pdf kinase-mediated signaling acute myocardial infarction coronary microembolization induced 200 mg kg−1 day−1 pdtc reflow phenomenon related chronic coronary microembolization heart failure induced check access instant access privacy choices/manage cookies acute coronary syndrome percutaneous coronary interventions liu sf perfusion–contraction mismatch myocardial infarction redefined reducing myocardial infarction

Questions {❓}

• Schulz R, Heusch G (2009) Tumor necrosis factor-α and its receptors 1 and 2 yin and yang in myocardial infarction?

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         description:The objective of this study was to evaluate the effects of specific NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) on inflammatory response and cardiac function in a rat model of coronary microembolization (CME). CME was developed by injecting a suspension of microthrombotic particles (MTPs) into the left ventricle when obstructing the ascending aorta. MTPs were generated from the rat clots sized by filtration through 38 μm screen. Thirty-two Sprague–Dawley rats served as sham group, 128 CME rats were randomized to untreated (CMEU) and PDTC-treated (CMEp) group. Rats in CMEp were administered intraperitoneally with 50, 100, 200 mg kg−1 day−1 PDTC, respectively, from 1 h before to 7 days after operation. The rats were sacrificed on day 1, 3, 7, 14 post-operationally and each subgroup consisted of eight rats. The general morphological characteristics were observed in sections with HE staining, and the severity of myocardial loss (SML) was determined by percent micro-necrotic area in sections with hematoxylin basic fuchsin picric (HBFP) staining 1 day or by percent micro-fibrotic area in sections with Masson’s trichrome staining 14 days post-operationally. Left ventricular (LV) function was evaluated echocardiographically and hemodynamically. Activity of NF-κB/DNA-binding was analyzed by electrophoresis mobility shift assays (EMSA), and expressions of TNF-α, IL-6, and ICAM-1 genes and proteins were detected by Real-time PCR and western blots, respectively. CME rats exhibited pathological changes evidenced by multi-focal myocardial necrosis, inflammatory cell infiltration with remarkably increased SML and persistent reduction of LV function. Activity of NF-κB/DNA-binding was markedly increased, also TNF-α, IL-6 and ICAM-1 transcripts and their protein expressions were upregulated strongly in the myocardium following CME. PDTC in a dose-dependency significantly suppressed the myocardial inflammatory cytokine transcriptions, decreased SML and improved LV function. Thus, NF-κB is markedly activated in CME hearts, and inhibition of NF-κB by PDTC prevents the subsequent inflammatory activation and improves cardiac function. Patients with or at risk of CME may benefit from acute anti-inflammatory treatment with PDTC.
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            Interleukin-6
            Intercellular adhesion molecule-1
            Pyrrolidine dithiocarbamate
            Cardiology
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      headline:Blockade of NF-κB by pyrrolidine dithiocarbamate attenuates myocardial inflammatory response and ventricular dysfunction following coronary microembolization induced by homologous microthrombi in rats
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         Coronary microembolization
         Nuclear factor-κB
         Tumor necrosis factor-α
         Interleukin-6
         Intercellular adhesion molecule-1
         Pyrrolidine dithiocarbamate
         Cardiology
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