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

Abstract

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.

• Authors: Cibele Canal Castro, Aline S Pagnussat, Nathalia Moura, Maira J da Cunha, Fernanda R Machado, Angela T S Wyse, Carlos Alexandre Netto
• Journal: Neurological research (Neurol Res) Vol. 36 Issue 3 Pg. 198-206 (Mar 2014) ISSN: 1743-1328 [Electronic] England
• PMID: 24512013 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Neuroprotective Agents
• Sodium-Potassium-Exchanging ATPase
• Coumestrol

Topics

• Animals
• Brain Ischemia (drug therapy, enzymology, pathology)
• CA1 Region, Hippocampal (drug effects, pathology)
• Cell Death
• Coumestrol (therapeutic use)
• Male
• Neuroprotective Agents (therapeutic use)
• Pyramidal Cells (drug effects)
• Rats
• Rats, Wistar
• Sodium-Potassium-Exchanging ATPase (metabolism)