Differences in brain edema and intracranial pressure following traumatic brain injury across the estrous cycle: Involvement of female sex steroid hormones

Maghool, Fatemeh; Khaksari, Mohammad; Khachki, Ali Siahposht

doi:10.1016/j.brainres.2012.12.014

Cited by 61 publications

(42 citation statements)

References 74 publications

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“…Multiple studies have reported PROG's edema-attenuating effects in a number of animal models of brain injury (Guo et al, 2006;Maghool et al, 2013). An inverse correlation between serum PROG level and degree of edema has been reported (Wright et al, 2001).…”

Section: Discussionmentioning

confidence: 97%

Evaluating the neurotherapeutic potential of a water-soluble progesterone analog after traumatic brain injury in rats

et al. 2016

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Section: Discussionmentioning

confidence: 97%

Evaluating the neurotherapeutic potential of a water-soluble progesterone analog after traumatic brain injury in rats

et al. 2016

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“…Evidence suggests that shifts in the hormonal milieu are associated with changes in risk/outcome. Protection from TBI in the rodent has been reported in proestrous phase (Maghool et al, 2013) when estrogen levels are increasing, although not all studies have replicated this effect (Wagner et al, 2004). Further supporting this hypothesis is the finding that the protective female advantage on outcome measures, such as a reduction of BBB permeability and cerebral edema, was attenuated or even completely absent in Ovx-induced surgically hormone-deplete rats (Bramlett and Dietrich, 2001; Suzuki et al, 2004).…”

Section: Estrogen Neuroprotection In Brain Injurymentioning

confidence: 99%

Estrogens as neuroprotectants: Estrogenic actions in the context of cognitive aging and brain injury

Engler-Chiurazzi

Brown

Povroznik

et al. 2017

Progress in Neurobiology

170

121

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There is ample empirical evidence to support the notion that the biological impacts of estrogen extend beyond the gonads to other bodily systems, including the brain and behavior. Converging preclinical findings have indicated a neuroprotective role for estrogen in a variety of experimental models of cognitive function and brain insult. However, the surprising null or even detrimental findings of several large clinical trials evaluating the ability of estrogen-containing hormone treatments to protect against age-related brain changes and insults, including cognitive aging and brain injury, led to hesitation by both clinicians and patients in the use of exogenous estrogenic treatments for nervous system outcomes. That estrogen-containing therapies are used by tens of millions of women for a variety of health-related applications across the lifespan has made identifying conditions under which benefits with estrogen treatment will be realized an important public health issue. Here we provide a summary of the biological actions of estrogen and estrogen-containing formulations in the context of aging, cognition, stroke, and traumatic brain injury. We have devoted special attention to highlighting the notion that estrogen appears to be a conditional neuroprotectant whose efficacy is modulated by several interacting factors. By developing criteria standards for desired beneficial peripheral and neuroprotective outcomes among unique patient populations, we can optimize estrogen treatments for attenuating the consequences of, and perhaps even preventing, cognitive aging and brain injury.

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“…Edema formation and intracranial pressure after TBI vary according to the estrus cycle [18]. Progesterone reduces lipid peroxidation and suppresses neuronal hyperexcitability, leading to membrane stabilization [35].…”

Section: Introductionmentioning

confidence: 99%

COX-2 regulation and TUNEL-positive cell death differ between genders in the secondary inflammatory response following experimental penetrating focal brain injury in rats

et al. 2015

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COX-2 regulation differed between genders after TBI. The increased COX-2 expression in male rats correlated with increased apoptotic cell death detected by increased TUNEL staining at 24 h, but not with neuronal necrosis measured by Flouro-Jade. Astrogliosis and microgliosis did not differ, confirming a comparable level of trauma. The gender-specific trait of the secondary inflammatory response may be connected to prostaglandin regulation, which may partially explain gender variances in outcome after TBI.

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Differences in brain edema and intracranial pressure following traumatic brain injury across the estrous cycle: Involvement of female sex steroid hormones

Cited by 61 publications

References 74 publications

Evaluating the neurotherapeutic potential of a water-soluble progesterone analog after traumatic brain injury in rats

Evaluating the neurotherapeutic potential of a water-soluble progesterone analog after traumatic brain injury in rats

Estrogens as neuroprotectants: Estrogenic actions in the context of cognitive aging and brain injury

COX-2 regulation and TUNEL-positive cell death differ between genders in the secondary inflammatory response following experimental penetrating focal brain injury in rats

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