[Neuroprotective effect of cerebrocurin in a model of acute cerebral stroke].
Chronic administration of cerebrocurin and cerebrolysin to Mongolian jirds with acute cerebral stroke model led to a decrease in the mitochondrial dysfunction on the 4th day, which was manifested by their ability to inhibit the mitochondrial permeability transition pore opening, normalize the energy metabolism, and enhance c-fos gene expression. In addition, cerebrocurin restored the morphofunctional state of neurons and favored the cell loss mechanism switching from necrosis to apoptosis. With respect to all characteristics under consideration, the effect of cerebrocurin exceeded with statistical confidence that of cerebrolysin.
Belenichev
I F
IF
Pavlov
S V
SV
Dunaev
V V
VV
D000208:Acute Disease; D000596:Amino Acids / Q000627:therapeutic use; D000818:Animals; D017209:Apoptosis; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D045424:Complex Mixtures; D004734:Energy Metabolism / Q000187:drug effects; D005849:Gerbillinae; D008928:Mitochondria / Q000502:physiology; D009336:Necrosis; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D009479:Neuropeptides / Q000627:therapeutic use*; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D020521:Stroke / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*
D000596:Amino Acids; D045424:Complex Mixtures; D009479:Neuropeptides; D018696:Neuroprotective Agents; D016760:Proto-Oncogene Proteins c-fos; C549026:cerebrocurin; C006952:cerebrolysin