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Neuroprotective activity of dimer of 16,16′-dimethyl-15-dehydroprostaglandin B 1 (di-Calciphor) in cerebral ischemia
Journal article   Peer reviewed

Neuroprotective activity of dimer of 16,16′-dimethyl-15-dehydroprostaglandin B 1 (di-Calciphor) in cerebral ischemia

Rick C.S. Lin, Diane F. Matesic, Robert J. McKenzie, Thomas M. Devlin and Dag K.J.E. von Lubitz
Brain research, v 606(1), pp 130-134
1993

Abstract

Calpain Cerebral ischemia Di-Calciphor Neuroprotection Prostaglandin B 1
Post-ischemic treatment of di-Calciphor (16,16′-dimethyl-15-dehydroprostaglandin B 1) 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.

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