Coumestrol treatment prevents Na+, K+-ATPase inhibition and affords histological neuroprotection to male rats receiving cerebral global ischemia

Objective: In this study, we investigated the possible mechanisms underlying the neuroprotective effects of coumestrol, a potent isoflavonoid with antioxidant activities and binding affinities for both estrogen receptors (ER) ER-alpha and ER-beta that are comparable to those of 17beta-estradiol, in...

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Published in:Neurological research (New York) 2014-03, Vol.36 (3), p.198-206
Main Authors: Castro, Cibele Canal, Pagnussat, Aline S., Moura, Nathalia, da Cunha, Maira J., Machado, Fernanda R., Wyse, Angela T. S., Netto, Carlos Alexandre
Format: Article
Language:English
Subjects:
Animals
ATPase
Brain Ischemia - drug therapy
Brain Ischemia - enzymology
Brain Ischemia - pathology
CA1 Region, Hippocampal - drug effects
CA1 Region, Hippocampal - pathology
Cell Death
Cerebral ischemia
Coumestrol
Coumestrol - therapeutic use
Hippocampus
Male
Neuroprotection
Neuroprotective Agents - therapeutic use
Pyramidal Cells - drug effects
Rats
Rats, Wistar
Sodium-Potassium-Exchanging ATPase - metabolism
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Summary:Objective: In this study, we investigated the possible mechanisms underlying the neuroprotective effects of coumestrol, a potent isoflavonoid with antioxidant activities and binding affinities for both estrogen receptors (ER) ER-alpha and ER-beta that are comparable to those of 17beta-estradiol, in a model of global ischemia in male subjects. Methods: Wistar rats underwent global ischemia (10 minutes) or sham surgery and received a single intracerebroventricular (icv) infusion of 20 μg of coumestrol or vehicle 1 hour before ischemia or 0, 3, 6, or 24 hours after reperfusion. Results: The data analysis revealed an extensive neuronal death in the CA1 hippocampal subfield at 7 days, and a significant decrease in the Na + , K + -ATPase activity at 1 and 24 hours after ischemia, and both injuries were attenuated by coumestrol administration. Conclusions: Coumestrol treatment was effective in preventing neuronal loss in all times of administration as well as able to rescue the Na + , K + -ATPase activity, suggesting its potential benefits for either prevention or therapeutics use against cerebral ischemia in males.
ISSN:0161-6412
1743-1328
DOI:10.1179/1743132813Y.0000000286