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Update of the Stroke Therapy Academic Industry Roundtable Preclinical Recommendations
The updated STAIR preclinical recommendations reinforce the previous suggestions that reproducibly defining dose response and time windows with both histological and functional outcomes in multiple animal species with appropriate physiological monitoring is appropriate.
Inflammatory Mediators and Stroke: New Opportunities for Novel Therapeutics
The realization that brain ischemia and trauma elicit robust inflammation in the brain provides fertile ground for discovery of novel therapeutic agents for stroke and neurotrauma and inhibition of the mitogen-activated protein kinase (MAPK) cascade via cytokine suppressive anti-inflammatory drugs are most promising new opportunities.
Tumor necrosis factor-alpha. A mediator of focal ischemic brain injury.
These studies demonstrate that exogenous T NF-alpha exacerbates focal ischemic injury and that blocking endogenous TNF-alpha is neuroprotective, and also significantly reduced focal ischemia-induced brain injury.
Inflammation and Stroke: Putative Role for Cytokines, Adhesion Molecules and iNOS in Brain Response to Ischemia
- G. Zoppo, I. Ginis, J. Hallenbeck, C. Iadecola, Xinkang Wang, G. Feuerstein
- BiologyBrain pathology
- 1 January 2000
Key data are summarized in support for the possibility that inflammatory cells and mediators are important contributing and confounding factors in ischemic brain injury and suggest that novel therapeutic strategies may evolve from detailed research on some specific inflammatory factors.
Proteolytic Cascade Enzymes Increase in Focal Cerebral Ischemia in Rat
- G. Rosenberg, Milo Navratil, F. Barone, G. Feuerstein
- Biology, MedicineJournal of cerebral blood flow and metabolism…
- 1 May 1996
The time of appearance of gelatinase B suggests a role in secondary tissue damage and vasogenic edema, while gelatinase A may be involved in tissue repair.
Tumor necrosis factor-alpha expression in ischemic neurons.
These results represent the first demonstration that focal cerebral ischemia in rats results in elevated TNF-alpha mRNA and protein in ischemic neurons, and the neuronal expression of peptide appears to facilitate the infiltration of inflammatory cells that can further exacerbate tissue damage in cerebral waschemia and might contribute to increased sensitivity and risk in focal stroke.
Inhibition of p38 mitogen-activated protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion.
Results demonstrate that p38 MAPK plays a pivotal role in the signal transduction pathway mediating postischemic myocardial apoptosis and that inhibiting p38MAPK may attenuate reperfusion injury.
The Role of Inflammation and Cytokines in Brain Injury
Ischemic preconditioning and brain tolerance: temporal histological and functional outcomes, protein synthesis requirement, and interleukin-1 receptor antagonist and early gene expression.
PC is a powerful inducer of ischemic brain tolerance as reflected by preservation of brain tissue and motor function and the importance of protein synthesis in PC-induced IT is evaluated.
Inhibition of extracellular signal-regulated kinase enhances Ischemia/Reoxygenation-induced apoptosis in cultured cardiac myocytes and exaggerates reperfusion injury in isolated perfused heart.
The data taken together suggest that ERK plays a protective role, whereas p38 and JNK mediate apoptosis in cardiomyocytes subjected to ischemia/reoxygenation (I/R), and the dynamic balance of their activities is critical in determiningCardiomyocyte fate subsequent to reperfusional injury.