Endocrinology, doi:10.1210/en.2005-0693
Endocrinology Vol. 147, No. 2 683-686
Copyright © 2006 by The Endocrine Society
Dehydroepiandrosterone Sulfate Is Neuroprotective when Administered Either before or after Injury in a Focal Cortical Cold Lesion Model
Gabriella Juhász-Vedres1,
Éva Rózsa1,
Gabriella Rákos,
Márton B. Dobszay,
Zsolt Kis,
János Wölfling,
József Toldi,
Árpád Párducz and
Tamás Farkas
Departments of Comparative Physiology (G.J.-V., E.R., G.R., M.B.D., Z.K., J.T., T.F.) and Organic Chemistry (J.W.), University of Szeged, H-6726 Szeged, Hungary; and Institute of Biophysics (A.P.), Biological Research Center, H-6701 Szeged, Hungary
Address all correspondence and requests for reprints to: Tamás Farkas, Ph.D., Department of Comparative Physiology, University of Szeged, Közép fasor 52., H-6726 Szeged, Hungary. E-mail: tfarkas{at}bio.u-szeged.hu.
Dehydroepiandrosterone and its sulfate (DHEAS) are sex hormone precursors that exert marked neurotrophic and/or neuroprotective activity in the central nervous system. The present study evaluated the effects of DHEAS and 17ß-estradiol (E2) in a focal cortical cold lesion model, in which DHEAS (50 mg/kg, sc) and E2 (35 mg/kg, sc) were administered either as pretreatment (two subsequent injections 1 d and 1 h before lesion induction) or posttreatment (immediately after lesion induction). The focal cortical cold lesion was induced in the primary motor cortex by means of a cooled copper cylinder placed directly onto the cortical surface. One hour later, the animals were killed, the brains cut into 0.4-mm-thick slices, and the sections stained with 1% triphenyltetrazolium chloride. The volume of the hemispheric lesion was calculated for each animal. The results demonstrated that the lesion area was significantly attenuated in both the DHEAS- and E2- pre- and posttreated groups and that in the presence of letrozole, a nonsteroidal aromatase inhibitor, no neuroprotection was observed, suggesting that the beneficial effect of DHEAS on the cold injury might depend on the conversion of DHEAS to E2 within the brain. It is concluded that even a single posttraumatic administration of DHEAS may be of substantial therapeutic benefit in the treatment of focal brain injury with vasogenic edema.
Copyright © 2006 by The Endocrine Society