Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since our previous study demonstrated the exacerbation of acute myocardial ischemia/reperfusion (AMIR)-related arrhythmia by intratracheal instillation (IT) of diesel exhaust particles (DEP), the influence of IT with extracts of DEP in organic solvents on AMIR-related arrhythmia was examined in rats. Oxidative activity in a non-biological assay system and proinflammatory activity in mice of DEP extracts were examined. The dichloromethane-soluble fraction (DMSF) of DEP was further fractionated into n-hexane-soluble (n-HSF) and n-hexane-insoluble (n-HISF) fractions. The oxidative activities of the fractions evaluated by dithiothreitol assay were ranked as follows: n-HISF>DMSF>n-HSF. Twenty-one to 34 hr after IT, the AMIR experiment was performed. Exacerbation of AMIR-related arrhythmia and increased reperfusion-related mortality were observed only in rats treated with DMSF. In fact, n-HSF and n-HISF did not affect arrhythmia up to 5 mg/kg. Twelve hr after IT, a significant increase in neutrophil count was observed only with DMSF. The levels of granulocyte colony-stimulating factor and interleukin-6 in bronchoalveolar lavage fluid were significantly elevated in the group treated with DMSF, while neither, n-HSF nor n-HISF, affected the level of cytokines up to 5 mg/kg. In fact, tumor necrosis factor-alpha, IL-10 and granulocyte-macrophage colony-stimulating factor were unchanged with any of the fractions. In conclusion, exacerbation of AMIR-related arrhythmia by DMSF suggests the contribution of non-particle components of DEP to arrhythmia while the component contributed to the effects did not become clear. Furthermore, it is confirmed that exacerbation of AMIR-related arrhythmia is accompanied by an increased neutrophil count in the circulatory blood.
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PMID:The effects of organic extract of diesel exhaust particles on ischemia/reperfusion-related arrhythmia and on pulmonary inflammation. 1830 79

Myocardial ischemia needs an alternative treatment such as gene therapy for the direct protection of cardiomyocytes against necrosis or apoptosis and to prevent the development of myocardial fibrosis and cardiac dysfunction. Despite the utility of gene therapy, its therapeutic use is limited due to inadequate transfection in cardiomyocytes and difficulty in directing to ischemic myocardium. Here, we present a polymeric gene carrier that is capable of targeting ischemic myocardium, resulting in high localization within the ischemic zone of the left ventricle (LV) of an ischemia/reperfusion (I/R) rat model upon systemic administration. Cystamine bisacrylamide-diamino hexane (CD) polymer was modified with the ischemic myocardium-targeted peptide (IMTP) and D-9-arginine (9R) for dual effects of the homing to ischemic myocardium and enhanced transfection efficiency with minimized polymer use. Conjugation of IMTP and 9R to CD led to an increase in transfection under hypoxia and significantly reduced the amount of polymer required for high transfection. Finally, we confirmed targeting of IMTP-CD-9R/DNA polyplex to ischemic myocardium and enhanced gene expression in LV of the I/R rat after tail vein injection. This study provides a clue that gene therapy for the treatment of myocardial ischemia can be achieved by using homing peptide-guided gene delivery systems.
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PMID:Targeted gene delivery to ischemic myocardium by homing peptide-guided polymeric carrier. 2321 82

Endothelial cells initiated inflammation persisting in postmyocardial infarction needs to be controlled and moderated for avoiding fatal complications. Curcuma oil (C.oil, Herbal Medicament), a standardized hexane soluble fraction of Curcuma longa has possessed neuroprotective effect. However, its effect on myocardial ischemia/reperfusion (MI/RP) and endothelial cells remains incompletely defined. Here, using in vivo rat MI/RP injury model and in vitro cellular approaches using EA.hy926 endothelial cells, enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and myograph, we provide evidence that with effective regimen and preconditioning of rats with C.oil (250 mg/kg, PO), before and after MI/RP surgery protects rats from MI/RP-induced injury. C.oil treatment reduces left ventricular ischemic area and endothelial cell-induced inflammation, specifically in the ischemic region (*P < 0.0001) and improved endothelial function by reducing the expression of proinflammatory genes and adhesion factors on endothelial cells both in vitro and in vivo. Furthermore, mechanistic studies have revealed that C.oil reduced the expression of adhesion factors like E-selectin (#P = 0.0016) and ICAM-1 ($P = 0.0069) in initiating endothelial cells-induced inflammation. In line to the real-time polymerase chain reaction expression data, C.oil reduced the adhesion of inflammatory cells to endothelial cells as assessed by the interaction of THP-1 monocytes with the endothelial cells using flow-based adhesion and under inflammatory conditions. These studies provide evidence that salutary effect of C.oil on MI/RP could be achieved with pretreatment and posttreatment of rats, C.oil reduced MI/RP-induced injury by reducing the endothelial cell-mediated inflammation, specifically in the ischemic zone of MI/RP rat heart.
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PMID:Curcuma oil reduces endothelial cell-mediated inflammation in postmyocardial ischemia/reperfusion in rats. 2485 88