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Cell Mol Neurobiol. 2017 Apr;37(3):405-416. doi: 10.1007/s10571-016-0372-1. Epub 2016 Apr 8.

Effects of Estrogen and Phytoestrogen Treatment on an In Vitro Model of Recurrent Stroke on HT22 Neuronal Cell Line.

Author information

1
Department of Functional Biology. Physiology Area, University of Oviedo, Av. Julián Clavería, No. 6, 33006, Oviedo, Spain.
2
Department of Clinical Neuroscience and Rehabilitation, Sahlgrenska Academy, University of Gothenburg, Medicinaregatan 9A, Box 440, 413 90, Gothenburg, Sweden.
3
Unit of Transplants, Cell Therapy and Regenerative Medicine, Central University Hospital of Asturias, Av. Roma s/n, 33011, Oviedo, Spain.
4
Prostate Cancer Institute, National University of Ireland, Galway. Co, Galway, Ireland.
5
Service of Hematology, Central University Hospital of Asturias, Av/Roma s/n, 33011, Oviedo, Spain.
6
Department of Laboratory Medicine, Central University Hospital of Asturias, Av/Roma s/n, 33011, Oviedo, Spain.
7
Department of Functional Biology. Physiology Area, University of Oviedo, Av. Julián Clavería, No. 6, 33006, Oviedo, Spain. tinog@uniovi.es.

Abstract

An increase of stroke incidence occurs in women with the decline of estrogen levels following menopause. This ischemic damage may recur, especially soon after the first insult has occurred. We evaluated the effects of estrogen and phytoestrogen treatment on an in vitro recurrent stroke model using the HT22 neuronal cell line. HT22 cells were treated with 17β-estradiol or genistein 1 h after the beginning of the first of two oxygen and glucose deprivation/reoxygenation (OGD/R) cycles. During the second OGD, there was a deterioration of some components of the electron transport chain, such as cytochrome c oxidase subunit 1 with a subsequent increase of reactive oxygen species (ROS) production. Accordingly, there was also an increase of apoptotic phenomena demonstrated by poly(ADP-ribose) polymerase 1 cleavage, Caspase-3 activity, and Annexin V levels. The recurrent ischemic injury also raised the hypoxia-inducible factor 1α and glucose transporter 1 levels, as well as the ratio between the lipidated and cytosolic forms of microtubule-associated protein 1A/1B-light chain 3 (LC3-II/LC3-I). We found a positive effect of estradiol and genistein treatment by partially preserving the impaired cell viability after the recurrent ischemic injury; however, this positive effect does not seem to be mediated neither by blocking apoptosis processes nor by decreasing ROS production. This work contribute to the better understanding of the molecular mechanisms triggered by recurrent ischemic damage in neuronal cells and, therefore, could help with the development of an effective treatment to minimize the consequences of this pathology.

KEYWORDS:

17β-estradiol; Apoptosis; Genistein; HT22 cells; Oxidative metabolism; Recurrent stroke

PMID:
27059741
DOI:
10.1007/s10571-016-0372-1
[Indexed for MEDLINE]

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