FR 167653

01/01/2000 - "In this report we investigated the dose of FR167653 effective in pulmonary ischemia-reperfusion injury in a canine model. "
06/01/1999 - "It is concluded that FR167653 appears to be effective in protecting the brain from ischemia-reperfusion injury after RCP.http://link.springer-ny.com/link/service/journals/00547/bibs/8n3p143.html"
02/01/1999 - "FR167653 ameliorates pulmonary ischemia-reperfusion injury."
11/01/1998 - "FR167653 ameliorates pulmonary ischemia-reperfusion injury in dogs."
04/01/2000 - "We designed this experimental study to evaluate the effect of FR167653 on ischemia-reperfusion injury of the rat lung. "

01/01/2000 - "In a previous study, we reported the efficacy of FR167653 in canine ischemia-reperfusion models. "
11/01/2004 - "Studies were performed with isolated, Langendorff-perfused Lewis rat hearts (n=80) which were either treated with FR167653 or untreated, as the control group, and subjected to ischemia-reperfusion. "
08/01/1998 - "In this study, we evaluated the effect of FR167653 in an extended liver resection with ischemia in a dog model. "
03/01/2009 - "After measuring the baseline hemodynamic parameters, including cardiac output (CO), left ventricular pressure (LVP), and maximum and minimum rates of increase in LVP (+/- LVdp/dt), FR167653 was administered continuously for 30 minutes before ischemia in the FR-1 and FR-2 groups. "
09/01/2004 - "Animals were divided into two groups: a control group (n = 5) subjected to 2-hour small bowel ischemia only, and a combination therapy group (FK/FR group, n = 5) that received FK409 (300 mcg/kg/h) plus FR167653 (1 mg/kg/h) intravenously before and after the ischemic event. "

08/01/2004 - "Liver histopathological examination showed FR167653 (100, 150 mg/kg) significantly reduced inflammatory cells infiltration and liver cells necrosis. "
03/01/2002 - "FR167653 significantly decreased cell infiltration into outer medulla, and the extent of acute tubular necrosis 24 and 48 h after reperfusion. "
09/01/2004 - "Adding to this, our study demonstrated that FR167653 prevented renal failure, such as the infiltration of inflammatory cells and tubular cell necrosis after hemorrhage, and the intestinal barrier damage was also dramatically improved by FR167653 treatment. "
03/01/2002 - "FR167653 markedly decreased the transcription of interleukin-1beta, tumour necrosis factor-alpha, monocyte chemoattractant protein-1 and regulated upon activation, normal T cell expression and secreted in diseased kidneys. "
12/01/1999 - "Both dexamethasone and FR167653 (an inhibitor of interleukin-1 beta/tumour necrosis factor-alpha production) also reduced the severity of intestinal lesions as well as the increase in iNOS activity following administration of indomethacin. "

12/01/2001 - "FR167653 might locally affect arthritic joints to prevent inflammation. "
08/01/2000 - "In addition, there was marked reduction in renal injury even when FR167653 treatment was initiated after glomerular inflammation was established, suggesting that the therapeutic application of FR167653 may be clinically useful for human renal diseases."
01/01/2012 - "FR167653 inhibited the inflammation-related hepatic injury following hemorrhagic shock. "
01/01/2012 - "Compared with either agent alone, a combination of fasudil and FR167653 was more effective for the improvement of myocardial damage, inflammation and oxidative stress. "
06/01/2004 - "We measured the expression levels of genes and proteins related to inflammation in human vascular smooth muscle cells (hVSMCs) treated with hemolysate and FR167653 (FR) (1 micromol/L), a selective p38MAPK inhibitor, for 48 hours by TaqMan real-time reverse transcription-polymerase chain reaction (RT-PCR) and ELISA. "

11/01/2005 - "In this study, our aim was to evaluate the role of p38 MAPK on the renal damage during the first 5 h after a hemorrhage using a specific inhibitor of p38 MAPK activation, FR167653. "
09/01/2004 - "Adding to this, our study demonstrated that FR167653 prevented renal failure, such as the infiltration of inflammatory cells and tubular cell necrosis after hemorrhage, and the intestinal barrier damage was also dramatically improved by FR167653 treatment. "
09/01/2007 - "Therefore, in this study, the role of p38 MAPK on cardiac dysfunction after hemorrhagic shock was studied up to 5 h after a hemorrhage using FR167653, a specific inhibitor of p38 MAPK phosphorylation. "