Neuroprotective activity of dimer of 16,16'-dimethyl-15-dehydroprostaglandin B1 (di-Calciphor) in cerebral ischemia.
Post-ischemic treatment of di-Calciphor (16,16'-dimethyl-15- dehydroprostaglandin B1) significantly improves animal survival and prevents ischemia-induced neurodegeneration of vulnerable forebrain regions assessed with histochemical and biochemical techniques in gerbils. Neuronal degeneration seen by Cresyl violet staining and silver impregnation in the CA1 sector of the hippocampus and the dorso-lateral sector of the striatum was significantly reduced in animals treated with di-Calciphor. In addition, the early onset of selective degradation of calpain I substrates spectrin and microtubule-associated protein (MAP2) in these same vulnerable regions was prevented. The lack of adverse side effects may facilitate the potential therapeutic use of this drug in preventing neuronal damage caused by stroke.
Lin
R C
RC
Department of Physiology and Biophysics, Hahnemann University, Philadelphia, PA 19102.
Matesic
D F
DF
McKenzie
R J
RJ
Devlin
T M
TM
von Lubitz
D K
DK
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology*; D003342:Corpus Striatum / Q000378:metabolism; D005849:Gerbillinae; D006624:Hippocampus / Q000378:metabolism; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009410:Nerve Degeneration / Q000187:drug effects; D011456:Prostaglandins B / Q000494:pharmacology*; D012039:Regional Blood Flow / Q000187:drug effects; D015424:Reperfusion; D013049:Spectrin / Q000378:metabolism
D008869:Microtubule-Associated Proteins; D011456:Prostaglandins B; D013049:Spectrin; C076722:di-Calciphor