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Dipyridamole protects cultured rat embryonic cortical neurons from neurotoxic insult
Author(s) -
Blake A. D.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.81.s1.40_7.x
Subject(s) - glutathione , dipyridamole , oxidative stress , buthionine sulfoximine , pharmacology , biology , endogeny , endocrinology , medicine , microbiology and biotechnology , neuroscience , biochemistry , enzyme
The effects of a clinically useful cardiovascular agent, dipyridamole, were examined in a rodent tissue culture model of neural protection. Dipyridamole effectively protected rat embryonic day 18 (E18) cortical neurons from either trophic deprivation or endogenous glutathione depletion by l ‐buthionine (R,S) sulfoximine (BSO). Trophic deprivation was associated with an increase in intracellular oxidative stress, as determined by the increased fluorescence of dichloro, dihydrofluorescein (H2DCFDA). Dipyridamole's neural protection was time and concentration‐dependent (EC50 = 342 n m ), and its continuous presence in the culture medium was required. Dipyridamole or exogenously added glutathione markedly decreased trophic deprivation induced H2DCFDA fluorescence, indicating a reduction in neuronal oxidative stress. These results demonstrate that dipyridamole protects primary neuronal cultures against either trophic or chemically mediated insults, and suggest that dipyridamole has a potent antioxidant ability that compensates for glutathione depletion in primary neuronal cells.