Literature DB >> 11283401

Estrogens decrease reperfusion-associated cortical ischemic damage: an MRI analysis in a transient focal ischemia model.

J Shi1, J D Bui, S H Yang, Z He, T H Lucas, D L Buckley, S J Blackband, M A King, A L Day, J W Simpkins.   

Abstract

BACKGROUND AND
PURPOSE: Early identification of irreversible cerebral ischemia is critical in defining strategies that influence neuronal survival after stroke. We used MRI to investigate the effects of 17beta-estradiol (E2) on the temporal evolution of focal ischemia.
METHODS: Female rats were ovariectomized and divided into 1 of 2 groups: ovariectomy alone (OVX; n=4) or ovariectomy with estrogen replacement (OVX+E2; n=3). Both groups were then subjected to 1-hour middle cerebral artery occlusion (MCAO), with the use of a standardized endovascular monofilament model, followed by reperfusion. Sequential diffusion-weighted (DWI) and T2-weighted (T2WI) MRI were obtained during and after the MCAO. In separate groups of animals (n=5 for OVX and OVX+E2), cerebral blood flow (CBF) was measured by laser-Doppler methods before, during, and after occlusion.
RESULTS: DWI detected similar lesion characteristics during MCAO in both groups. In the OVX group, lesion size did not change during reperfusion, but the signal intensity ratio increased early and stabilized during the latter stages. In contrast, DWI lesion size decreased during reperfusion in OVX+E2 rats by 50% to 60% (P<0.05), a size reduction almost exclusively limited to cortical regions. During MCAO, the signal intensity ratio in OVX+E2 rats was reduced compared with OVX rats. Reperfusion further attenuated the signal intensity ratio in cortical but not subcortical regions (P<0.05 versus OVX). T2WI revealed no lesions in either group during MCAO, but it detected lesion sizes similar to that of DWI during reperfusion. Furthermore, similar patterns and magnitudes of estrogen treatment-related decrease in lesion size were noted after reperfusion. T2WI demonstrated less intense signal intensity ratio changes in both groups compared with DWI. There were no differences in CBF between groups either during occlusion, early reperfusion, or 1 day after reperfusion.
CONCLUSIONS: This study strongly suggests that estrogens selectively protect cortical tissue from ischemic damage during MCAO and that this protection is exerted during both the occlusion and reperfusion phases of ischemia and does not involve an estrogen-related change in CBF.

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Year:  2001        PMID: 11283401     DOI: 10.1161/01.str.32.4.987

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  15 in total

Review 1.  Neurotrophic and neuroprotective actions of estrogen: basic mechanisms and clinical implications.

Authors:  Darrell W Brann; Krishnan Dhandapani; Chandramohan Wakade; Virendra B Mahesh; Mohammad M Khan
Journal:  Steroids       Date:  2007-02-21       Impact factor: 2.668

Review 2.  PELP1: a key mediator of oestrogen signalling and actions in the brain.

Authors:  R Thakkar; G R Sareddy; Q Zhang; R Wang; R K Vadlamudi; D Brann
Journal:  J Neuroendocrinol       Date:  2018-02       Impact factor: 3.627

Review 3.  The assessment of non-feminizing estrogens for use in neuroprotection.

Authors:  Kun Don Yi; Evelyn Perez; Shaohua Yang; Ran Liu; Douglas F Covey; James W Simpkins
Journal:  Brain Res       Date:  2010-11-25       Impact factor: 3.252

4.  Dose dependence and therapeutic window for the neuroprotective effects of 17beta-estradiol when administered after cerebral ischemia.

Authors:  Ran Liu; Xiaofei Wang; Qing Liu; Shao-Hua Yang; James W Simpkins
Journal:  Neurosci Lett       Date:  2007-02-14       Impact factor: 3.046

Review 5.  Neuroprotection with non-feminizing estrogen analogues: an overlooked possible therapeutic strategy.

Authors:  James W Simpkins; Timothy E Richardson; Kun Don Yi; Evelyn Perez; Douglas F Covey
Journal:  Horm Behav       Date:  2012-04-03       Impact factor: 3.587

Review 6.  Estrogens and progesterone as neuroprotectants: what animal models teach us.

Authors:  Meharvan Singh; Nathalie Sumien; Cheryl Kyser; James W Simpkins
Journal:  Front Biosci       Date:  2008-01-01

7.  Quinol-based cyclic antioxidant mechanism in estrogen neuroprotection.

Authors:  Laszlo Prokai; Katalin Prokai-Tatrai; Pal Perjesi; Alevtina D Zharikova; Evelyn J Perez; Ran Liu; James W Simpkins
Journal:  Proc Natl Acad Sci U S A       Date:  2003-09-22       Impact factor: 11.205

Review 8.  Estrogen and selective estrogen receptor modulators: neuroprotection in the Women's Health Initiative era.

Authors:  Stephanie Murphy; Louise McCullough; Marguerite Littleton-Kearney; Patricia Hurn
Journal:  Endocrine       Date:  2003-06       Impact factor: 3.633

Review 9.  Estrogen actions on mitochondria--physiological and pathological implications.

Authors:  James W Simpkins; Shao-Hua Yang; Saumyendra N Sarkar; Virginia Pearce
Journal:  Mol Cell Endocrinol       Date:  2008-05-02       Impact factor: 4.102

10.  High-dose estrogen treatment at reperfusion reduces lesion volume and accelerates recovery of sensorimotor function after experimental ischemic stroke.

Authors:  Randall S Carpenter; Ifeanyi Iwuchukwu; Cyrus L Hinkson; Sydney Reitz; Wonhee Lee; Ayaka Kukino; An Zhang; Martin M Pike; Agnieszka A Ardelt
Journal:  Brain Res       Date:  2016-03-17       Impact factor: 3.252

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