Inflammation and apoptosis: linked therapeutic targets in spinal cord injury.
The secondary cascade of cell death that follows central nervous system (CNS) injury or ischemia has long been considered a target for neuroprotective agents aimed at sparing tissue and function. Recently, several laboratories have shown remarkable protection and recovery of function in rodent models of spinal cord injury using treatments that target components of the CNS inflammatory response. The use of minocycline, an antibiotic that reduces microglial activation, antibody blockade of the CD95 (FAS) ligand and the blockade of glycosphingolipid-induced iNOS (inducible nitric oxide synthase) have recently been shown to reduce neuronal and glial apoptosis with concomitant improvement in neurological function, and appear to enhance the efficacy of cell transplantation strategies.
Beattie
Michael S
MS
Spinal Trauma and Repair (STAR) Laboratories, Neurobiology of Disease Institute and Department of Neuroscience, The Ohio State University Medical Center, Columbus, OH 43210, USA. Beattie.2@osu.edu
D000818:Animals; D000906:Antibodies / Q000627:therapeutic use; D017209:Apoptosis; D007249:Inflammation / Q000188:drug therapy / Q000503:physiopathology; D017628:Microglia / Q000502:physiology; D008911:Minocycline / Q000627:therapeutic use; D017942:Nitric Acid / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052247:Nitric Oxide Synthase Type II; D051381:Rats; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D019014:fas Receptor / Q000502:physiology
D000906:Antibodies; D014409:Tumor Necrosis Factor-alpha; D019014:fas Receptor; D017942:Nitric Acid; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D008911:Minocycline