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17β-estradiol and inflammation: implications for ischemic stroke.

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Although typically associated with maintenance of female reproductive function, estrogens mediate physiological processes in nearly every body tissue, including the central nervous system. Numerous pre-clinical studies have shown that estrogen, specifically 17-beta-estradiol (17β-E2), protects the

Estrogen enhances neurogenesis and behavioral recovery after stroke.

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Stroke is a leading cause of permanent disability and death. It is well accepted that the principal mammalian estrogen (E2), 17-β estradiol, provides robust neuroprotection in a variety of brain injury models in animals of both sexes. E2 enhances neurogenesis after stroke in the subventricular zone;

Effect of growth factors on DNA labeling and cytoskeletal protein expression in 17-beta-estradiol and basic fibroblast growth factor pre-treated astrocyte cultures.

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Astrocytes react to all noxae which damage neurons. Their reactions include degeneration, hypertrophy, hyperplasia and fibre formation. Growth factors inducing proliferation and differentiation of both neurons and astrocytes in culture play a pivotal role in the dynamic flow of signaling molecules

Relaxant effects of 17-beta-estradiol in cerebral arteries through Ca(2+) entry inhibition.

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Estrogens account for gender differences in the incidence and outcome of stroke, but it remains unclear to what extent neuroprotective effects of estrogens are because of parenchymal or vascular actions. Because reproductive steroids have vasoactive properties, the authors assessed the effects and

17-beta-estradiol induces heat shock proteins in brain arteries and potentiates ischemic heat shock protein induction in glia and neurons.

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Estradiol reduces brain injury from many diseases, including stroke and trauma. To investigate the molecular mechanisms of this protection, the effects of 17-beta-estradiol on heat shock protein (HSP) expression were studied in normal male and female rats and in male gerbils after global ischemia.

Effects of 15 months of 17 beta-estradiol and dydrogesterone on systolic cardiac function according to quantitative and Doppler echocardiography in healthy postmenopausal women.

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OBJECTIVE Our goal was to investigate the short-term and intermediate effects of low-dose hormone replacement therapy on echocardiographic parameters of cardiac function in healthy postmenopausal women. METHODS In a prospective, controlled study 30 healthy postmenopausal women (mean age, 52 +/- 3

Stroke in the female: role of biological sex and estrogen.

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Women are protected from stroke relative to men until the years of menopause. Because stroke is the leading cause of serious, long-term disability in the United States, modeling sex-specific mechanisms and outcomes in animals is vital to research. Important research questions are focused on the

Hormone replacement therapy and stroke.

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Stroke is the third most common cause of death in women and a major cause of disability. Stroke occurs in older age in women compared with men. High premenopausal estrogen concentrations in women are thought to be protective against stroke and cardiovascular disease. Estrogens are essential for

Postischemic cerebral blood flow recovery in the female: effect of 17 beta-estradiol.

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Female reproductive hormones are considered to be protective agents in atherosclerotic vascular disease and stroke. The present study determined if there are unique cerebrovascular responses in female animals to global cerebral ischemia and if 17 beta-estradiol is important to postischemic outcome

17 β -Estradiol attenuates poststroke depression and increases neurogenesis in female ovariectomized rats.

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Studies have linked neurogenesis to the beneficial actions of specific antidepressants. However, whether 17 β -estradiol (E2), an antidepressant, can ameliorate poststroke depression (PSD) and whether E2-mediated improvement of PSD is associated with neurogenesis are largely unexplored. In the

Decreased serum testosterone in men with acute ischemic stroke.

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Serum levels of total and free testosterone and 17 beta-estradiol were determined in 144 men with acute ischemic stroke and 47 healthy male control subjects. Blood samples from patients were drawn a mean of 3 days after stroke onset and also 6 months after admission in a subgroup of 45 patients.

Purification and partial characterization of a 17 beta-estradiol-binding macromolecule in the human pancreas.

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Studies have been performed in order to investigate the presence of estrogen-binding proteins in the human pancreas that may provide the biochemical basis for tissue-specific treatment of pancreatic carcinoma with estrogen-based cytotoxic drugs. Using in vitro techniques, an estrogen-binding

17-beta estradiol inhibits oxidative stress-induced accumulation of AIF into nucleolus and PARP1-dependent cell death via estrogen receptor alpha.

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Oxidative stress-induced DNA damage results in over-activation of poly(ADP-ribose) polymerase 1 (PARP1), leading to parthanatos, a newly discovered cell elimination pathway. Inhibition of PARP1-dependent cell death has shown to improve the outcome of diseases, including stroke, heart ischemia, and

Estrogen attenuates over-expression of beta-amyloid precursor protein messager RNA in an animal model of focal ischemia.

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Cerebral ischemia is a risk factor for late onset Alzheimer's disease. Since estrogen replacement therapy benefits the outcome of cerebral stroke in post-menopausal women, we designed the present study to investigate the effects of estrogen on the expression of beta-amyloid precursor protein (APP)

The effect of the hypoestrogenic state, induced by gonadotropin-releasing hormone agonist, on Doppler-derived parameters of aortic flow.

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The effect of the hypoestrogenic state, induced by a GnRH agonist (GnRH-a), on cardiac function in healthy young women, was evaluated by Doppler echocardiography performed before treatment and when serum 17 beta-estradiol levels were suppressed by GnRH-a to 36.7 pmol/L. The following parameters of

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