Protective effects of estradiol in the brain of rats with genetic or mineralocorticoid-induced hypertension

Pietranera, Luciana; Saravia, Flavia; Roig, Paulina; Lima, Analı́a; Nicola, Alejandro F. De

doi:10.1016/j.psyneuen.2007.11.009

Cited by 25 publications

(55 citation statements)

References 84 publications

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“…Thus, a sign of estrogen neuroprotection relates to the positive control of neurogenesis. This possibility receives support from data showing that estradiol enhances neurogenesis under conditions of low cell proliferation, such as ischemic stroke, diabetes mellitus and aging (9,37).…”

Section: Estrogen Neuroprotection In Experimental Hypertensionmentioning

confidence: 90%

“…At the hypothalamic level, estradiol treatment normalized the high expression of arginine vasopressin (AVP) mRNA and of the V1 type AVP receptor shown by the steroid-untreated SHR or DOCAqsalt-treated groups (8,9). Figure 3 shows a pronounced immunolabeling of AVP mRNA in the dorsal and medial magnocellular cells of the paraventricular hypothalamic nucleus of SHR respect of WKY rats; furthermore, estradiol treatment normalized AVP mRNA in SHR, without an effect on WKY rats.…”

Section: Estrogen Neuroprotection In Experimental Hypertensionmentioning

confidence: 94%

“…The spontaneously hypertensive rat (SHR), a genetic model resembling human essential hypertension, is distinguished by hippocampal neuronal loss, astrogliosis with increased expression of the marker glial fibrillary acidic protein (GFAP), blood-brain barrier disruption, cytoskeletal breakdown, decreased forebrain white matter volume and abnormal neurogenesis (6)(7)(8)(9)(10). These changes made SHR models of dementia and the attention deficit hyperactivity syndrome (5).…”

Section: Introduction: Hypertension and Brain Damagementioning

confidence: 99%

“…These changes made SHR models of dementia and the attention deficit hyperactivity syndrome (5). The question remains if hippocampal changes are consequences of a pre-existing hypertension or whether hypertension and brain pathology reflect a central defect in this strain (8,9,11,12). Hormonal imbalances are frequent companions of hypertension.…”

Section: Introduction: Hypertension and Brain Damagementioning

confidence: 99%

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Protective effect of estrogens on the brain of rats with essential and endocrine hypertension

Nicola¹,

Pietranera²,

Bellini

et al. 2010

Hormone Molecular Biology and Clinical Investigation

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Estrogen neuroprotection has been shown in pathological conditions damaging the hippocampus, such as trauma, aging, neurodegeneration, excitotoxicity, oxidative stress, hypoglycemia, amyloid-β peptide exposure and ischemia. Hypertensive encephalopathy also targets the hippocampus; therefore, hypertension seems an appropriate circumstance to evaluate steroid neuroprotection. Two experimental models of hypertension, spontaneously hypertensive rats (SHR) and deoxycorticosterone (DOCA)-salt hypertensive rats, develop hippocampal abnormalities, which include decreased neurogenesis in the dentate gyrus, astrogliosis, low expression of brain-derived neurotrophic factor (BDNF) and decreased number of neurons in the hilar region, with respect of their normotensive strains Wistar Kyoto (WKY) and Sprague-Dawley rats. After estradiol was given for 2 weeks to SHR and DOCA-treated rats, both hypertensive models normalized their faulty hippocampal parameters. Thus, estradiol treatment positively modulated neurogenesis in the dentate gyrus of the hippocampus, according to bromodeoxyuridine incorporation and doublecortin immunocytochemistry, decreased reactive astrogliosis, increased BDNF mRNA and protein expression in the dentate gyrus and increased neuronal number in the hilar region of the dentate gyrus. A role of local estrogen biosynthesis is suggested in SHR, because basal aromatase mRNA in the hippocampus and immunoreactive aromatase protein in cell processes of the dentate gyrus were highly expressed in these rats. Estradiol further stimulated aromatase-related parameters in SHR but not in WKY. These observations strongly support that a combination of exogenous estrogens to those locally synthesized might better alleviate hypertensive encephalopathy. These studies broaden estrogen neuroprotective functions to the hippocampus of hypertensive rat models.

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Section: Estrogen Neuroprotection In Experimental Hypertensionmentioning

confidence: 90%

Section: Estrogen Neuroprotection In Experimental Hypertensionmentioning

confidence: 94%

Section: Introduction: Hypertension and Brain Damagementioning

confidence: 99%

Section: Introduction: Hypertension and Brain Damagementioning

confidence: 99%

See 2 more Smart Citations

Protective effect of estrogens on the brain of rats with essential and endocrine hypertension

Nicola¹,

Pietranera²,

Bellini

et al. 2010

Hormone Molecular Biology and Clinical Investigation

Self Cite

View full text Add to dashboard Cite

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“…35) CRH neurons in PVN were also reported to be hyper-activated in major depression. 36) Serotonin 5-HT 1A receptors, which are abundantly expressed in the brain, are thought to be essential for antidepressant responses. 37) 5-HT 1A receptors are involved in the pathophysiology of depression 38) and have been shown to act as targets for antidepressants in various in vivo models of depression.…”

Section: )mentioning

confidence: 99%

Antidepressant-Like Effects of Sanggenon G, Isolated from the Root Bark of <i>Morus alba</i>, in Rats: Involvement of the Serotonergic System

Lim

Jung

Park

et al. 2015

Biological & Pharmaceutical Bulletin

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The root bark of Morus alba is commonly used as an alternative medicine due to its numerous health benefits in humans. However, the antidepressant effects of various active components from M. alba have not been fully elucidated. In this study, we aimed to determine whether sanggenon G, an active compound isolated from the root bark of M. alba, exhibited antidepressant-like activity in rats subjected to forced swim test ( Key words Morus alba; sanggenon G; depression; serotonin; forced swim testDepression is a chronic disease that has an enormous impact on society. According to the predictions of the World Health Organization, by the year 2020, depression will be the second leading global burden of illness.1) Despite recent progress in the development of clinically relevant antidepressant drugs, currently available antidepressant are not totally effective and are associated with many undesirable adverse effects.2) Because of the limitations of antidepressant drugs, alternative approaches, such as medicinal herbs, have been studied for their potential applications in the treatment of depression.3,4) Moreover, many herbal extracts have been shown to have antidepressant effects in a variety of animal models. For example, Hypericum perforatum, also known as St. John's wort, is widely used for the treatment of mild to moderate depression. 5) Panax ginseng, commonly known as Korea Ginseng, has been investigated experimentally and clinically for its stress-attenuating activity. 6,7)The mulberry tree (Morus alba L.), one of the most wellknown and widely distributed trees of the family Moraceae, is extensively cultivated in East Asia; the leaves of M. alba L. are an indispensable food source for silkworms, and the fruits are consumed in normal diets.8) The root bark of M. alba is commonly known by the Chinese name of "Sang-Bai-Pi" and is widely used for its anti-inflammatory, antihypertensive, diuretic, and antipyretic effects. 9) M. alba extracts have also been reported to possess hypotensive, 10) hypoglycemic, 11) hepatoprotective, 12) neuroprotective, 13) and anti-inflammatory 14) activities. However, while M. alba extracts have been reported to exert antidepressant or antistress activities in various animal models, little is known about the antidepressant-like effects of active compounds from the root bark of M. alba extracts. [15][16][17][18] In the present study, the antidepressant-like effects of sanggenon G (Fig. 1), a major phenolic compound isolated from the ethyl acetate-soluble fraction of the root bark of M. alba, were investigated in response to the forced swim test (FST) in rats. Moreover, to determine the neurobiological effects underlying the antidepressant-like activity of the sanggenon G, corticosterone responses and c-Fos immunoreactivity were evaluated in rats exposed to FST.

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Aldosterone activates the oncogenic signals ERK1/2 and STAT3 via redox‐regulated mechanisms

Queisser

Schupp

Schwarz

et al. 2017

Molecular Carcinogenesis

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Epidemiological studies found an increased risk for kidney cancer in hypertensive patients, of which a subgroup has high aldosterone (Ald) levels. We recently showed that Ald is genotoxic both in kidney tubular cells and in rats with mineralocorticoid-mediated hypertension. The present work investigated in vitro and in vivo, if the oxidative stress-mediated activation of the ERK1/2 pathway, and its downstream target STAT3, could be one mechanism involved in the potential oncogenic capability of excess Ald exposure. The effects of excess Ald were investigated in LLC-PK1 cells and in Ald-induced hypertensive rats. Ald caused cRaf, MEK1/2, and ERK1/2 phosphorylation both in LLC-PK1 cells and in rat kidneys. ERK1/2 activation led to an increased phosphorylation of MSK1, p90RSK, and STAT3. The involvement of ERK1/2 in the activation of STAT3 was evidenced by the capacity of the MEK inhibitor U0126 to prevent Ald-mediated ERK1/2 and STAT3 phosphorylation.Both in vitro and in vivo, the activation of ERK1/2 and STAT3 by Ald was dependent on the mineralocorticoid receptor and was triggered by an increase in cellular oxidants. Ald-mediated oxidant increase was in part due to the activation of the enzymes NADPH oxidase and NO synthase. 1 On the other hand, we recently showed that excess Ald is genotoxic and causes oxidative stress in renal tubular cells 2,3 and in rat kidneys. [4][5][6] In hypertensive patients, epidemiological studies revealed higher cancer mortality and an increased risk to develop kidney cancer. 7-11Proposed underlying factors are the mitogenic effects of the blood pressure-regulating hormones angiotensin II and Ald. Abnormalities in apoptotic and proliferative processes associated with hypertension could lead to cellular overgrowth.

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Protective effects of estradiol in the brain of rats with genetic or mineralocorticoid-induced hypertension

Cited by 25 publications

References 84 publications

Protective effect of estrogens on the brain of rats with essential and endocrine hypertension

Protective effect of estrogens on the brain of rats with essential and endocrine hypertension

Antidepressant-Like Effects of Sanggenon G, Isolated from the Root Bark of <i>Morus alba</i>, in Rats: Involvement of the Serotonergic System

Aldosterone activates the oncogenic signals ERK1/2 and STAT3 via redox‐regulated mechanisms

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