Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carthamin yellow (CY) is a flavonoid compound isolated from safflower, which is widely used clinically in China. It has various pharmacological effects including promoting blood circulation to remove blood stasis and alleviating pain. Ischemic heart disease is one of the main culprits of illness and death. Here, in this study, ex vivo and in vivo models were used to investigate whether CY reduces ischemia/reperfusion injury. In vitro experiments further verify and explain the potential mechanisms of CY cardioprotective function. Isolated hearts from male rats with or without CY pretreatment before ischemia which underwent 30-minute ischemia followed by 60-minute reperfusion showed that CY pretreatment significantly reduced the infarct size and lactate dehydrogenase release. The in vivo experiments also indicated CY preadministration (i.v.) reduced infarct size and improved the heart function, which was impaired by myocardial ischemia/reperfusion injury. The in vitro model on myocardial cell also showed that CY reduced ischemia/reperfusion injury by reducing the lactate dehydrogenase and reactive oxygen species (ROS) releasing. Eliminating ROS with N-acetylcysteine or preinject CY into rat jugular vein reduces the expression of IL-6, TNF-a, and, especially, IL-1b in an in vivo I/R model. Also, CY pretreatment strongly reduces ischemia/reperfusion-induced NLRP3 up-expression and caspase-1 activation. Our results indicated CY reduced ischemia-reperfusion injury when administered before reperfusion. The reduction in injury is accompanied by a reduced ROS release and decreased inflammatory response.
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PMID:Carthamin Yellow Protects the Heart Against Ischemia/Reperfusion Injury With Reduced Reactive Oxygen Species Release and Inflammatory Response. 3135 40

Toll-like receptor 4 (TLR4) contributes to the pathogenesis of coronary ischemia/reperfusion (IR). To test whether the new TLR4 antagonist, ApTOLL, may prevent coronary IR damage, we administered 0.078 mg/kg ApTOLL or Placebo in pigs subjected to IR, analyzing the levels of cardiac troponins, matrix metalloproteinases, pro-, and anti-inflammatory cytokines, heart function, and tissue integrity over a period of 7 days after IR. Our results show that ApTOLL reduced cardiac troponin-1 24 h after administration, improving heart function, as detected by a significant recovery of the left ventricle ejection fraction (LVEF) and the shortening fraction (FS) cardiac parameters. The extension of necrotic and fibrotic areas was also reduced, as detected by Evans blue/2,3,5-triphenyltetrazolium chloride (TTC) staining, Hematoxylin/Eosine, and Masson Trichrome staining of heart sections, together with a significant reduction in the expression of the extracellular matrix-degrading, matrix metalloproteinase 9. Finally, the expression of the following cytokines, CCL1, CCL2, MIP1-A-B, CCL5, CD40L, C5/C5A, CXCL1, CXCL10, CXCL11, CXCL12, G-CSF, GM-CSF, ICAM-1, INF-g, IL1-a, ILI-b, IL-1Ra, IL2, IL4, IL5, IL6, IL8, IL10, IL12, IL13, IL16, IL17-A, IL17- E, IL18, IL21, IL27, IL32, MIF, SERPIN-E1, TNF-a, and TREM-1, were also assayed, detecting a pronounced decrease of pro-inflammatory cytokines after 7 days of treatment with ApTOLL. Altogether, our results show that ApTOLL is a promising new tool for the treatment of acute myocardial infarction (AMI).
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PMID:Targeting TLR4 with ApTOLL Improves Heart Function in Response to Coronary Ischemia Reperfusion in Pigs Undergoing Acute Myocardial Infarction. 3278 4


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