sb 239063 has been researched along with Cardiovascular Stroke in 8 studies
SB 239063: structure in first source
SB-239063 : A member of the class of imidazoles carrying 4-hydroxycyclohexyl, 4-fluorophenyl and 2-methoxypyrimidin-4-yl substituents at positions 1, 4 and 5 respectively.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Despite a reduction of inflammation, treatment with the p38 inhibitor SB 239063 does not affect cardiac remodelling and cardiac function when treatment is started 7 days after myocardial infarction." | 3.74 | Role of p38 mitogen-activated protein kinase in cardiac remodelling. ( Angermann, CE; Bauersachs, J; Behr, T; Ertl, G; Fraccarollo, D; Frantz, S; Goldberg, E; Hu, K; Strotmann, J, 2007) |
| "Adult male rats were subjected to 30 min ischemia and 4 (apoptosis assay) or 24 h (myocardial infarction determination) of reperfusion and treated with vehicle, SB 239063, insulin or insulin plus wortmannin." | 3.72 | Early anti-apoptosis treatment reduces myocardial infarct size after a prolonged reperfusion. ( Christopher, TA; Gao, E; Gao, F; Liu, HR; Lopez, BL; Ma, XL; Tao, L; Yan, W, 2004) |
| "PCADK holds great promise for treating myocardial infarction and other inflammatory diseases given its neutral, biocompatible degradation products and its ability to deliver a wide range of therapeutics." | 1.35 | Sustained release of a p38 inhibitor from non-inflammatory microspheres inhibits cardiac dysfunction. ( Brown, M; Davis, ME; Dikalov, S; Murthy, N; Oh, T; Seshadri, G; Sy, JC; Yang, SC, 2008) |
| "However, the effect of p38 MAPK on myocardial reperfusion injury, a pathologic condition involving a typical inflammatory response, has not been fully examined." | 1.31 | p38 MAPK inhibition reduces myocardial reperfusion injury via inhibition of endothelial adhesion molecule expression and blockade of PMN accumulation. ( Barone, FC; Christopher, TA; Gao, F; Lopez, BL; Ma, XL; Ohlstein, EH; Shi, DW; Yue, TL, 2002) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 6 (75.00) | 29.6817 |
| 2010's | 2 (25.00) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Sy, JC | 1 |
| Seshadri, G | 1 |
| Yang, SC | 1 |
| Brown, M | 2 |
| Oh, T | 1 |
| Dikalov, S | 1 |
| Murthy, N | 2 |
| Davis, ME | 2 |
| Gray, WD | 1 |
| Che, P | 1 |
| Ning, X | 1 |
| Levit, RD | 1 |
| Taylor, WR | 1 |
| Widder, J | 1 |
| Behr, T | 2 |
| Fraccarollo, D | 2 |
| Hu, K | 2 |
| Galuppo, P | 1 |
| Tas, P | 1 |
| Angermann, CE | 2 |
| Ertl, G | 2 |
| Bauersachs, J | 2 |
| Gao, F | 2 |
| Tao, L | 1 |
| Yan, W | 1 |
| Gao, E | 1 |
| Liu, HR | 1 |
| Lopez, BL | 2 |
| Christopher, TA | 2 |
| Ma, XL | 2 |
| Kaiser, RA | 1 |
| Lyons, JM | 1 |
| Duffy, JY | 1 |
| Wagner, CJ | 1 |
| McLean, KM | 1 |
| O'Neill, TP | 1 |
| Pearl, JM | 1 |
| Molkentin, JD | 1 |
| Frantz, S | 1 |
| Strotmann, J | 1 |
| Goldberg, E | 1 |
| Yue, TL | 1 |
| Shi, DW | 1 |
| Ohlstein, EH | 1 |
| Barone, FC | 1 |
8 other studies available for sb 239063 and Cardiovascular Stroke
| Article | Year |
|---|---|
Sustained release of a p38 inhibitor from non-inflammatory microspheres inhibits cardiac dysfunction.
Topics: Animals; Cell Line; Delayed-Action Preparations; Imidazoles; Macrophage Activation; Male; Mice; Mice | 2008 |
N-acetylglucosamine conjugated to nanoparticles enhances myocyte uptake and improves delivery of a small molecule p38 inhibitor for post-infarct healing.
Topics: Acetylglucosamine; Animals; Cardiovascular Agents; Drug Carriers; Imidazoles; Myocardial Infarction; | 2011 |
A clinical commentary on the article "N-acetylglucosamine conjugated to nanoparticles enhances myocyte uptake and improves delivery of a small molecule p38 inhibitor for post-infarct healing" : N-acetylglucosamine conjugated nanoparticles: translational o
Topics: Acetylglucosamine; Animals; Cardiovascular Agents; Chemistry, Pharmaceutical; Disease Models, Animal | 2011 |
Vascular endothelial dysfunction and superoxide anion production in heart failure are p38 MAP kinase-dependent.
Topics: Acetylcholine; Angiotensin-Converting Enzyme Inhibitors; Animals; Endothelium, Vascular; Heart Failu | 2004 |
Early anti-apoptosis treatment reduces myocardial infarct size after a prolonged reperfusion.
Topics: Androstadienes; Animals; Apoptosis; Disease Models, Animal; Imidazoles; Insulin; Male; Myocardial In | 2004 |
Inhibition of p38 reduces myocardial infarction injury in the mouse but not pig after ischemia-reperfusion.
Topics: Animals; Imidazoles; Mice; Myocardial Infarction; p38 Mitogen-Activated Protein Kinases; Pyrimidines | 2005 |
Role of p38 mitogen-activated protein kinase in cardiac remodelling.
Topics: Animals; Imidazoles; Inflammation; Male; Myocardial Infarction; p38 Mitogen-Activated Protein Kinase | 2007 |
p38 MAPK inhibition reduces myocardial reperfusion injury via inhibition of endothelial adhesion molecule expression and blockade of PMN accumulation.
Topics: Analysis of Variance; Animals; Endothelium, Vascular; Imidazoles; Intercellular Adhesion Molecule-1; | 2002 |