progesterone/stroke

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Progesterone attenuates hemorrhagic transformation after delayed tPA treatment in an experimental model of stroke in rats: involvement of the VEGF-MMP pathway.

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Tissue plasminogen activator (tPA) is the only FDA-approved treatment for acute stroke, but its use remains limited. Progesterone (PROG) has shown neuroprotection in ischemia, but before clinical testing, we must determine how it affects hemorrhagic transformation in tPA-treated ischemic rats. Male

Neurosteroids and Ischemic Stroke: Progesterone a Promising Agent in Reducing the Brain Injury in Ischemic Stroke.

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Progesterone (P4), a well-known neurosteroid, is produced by ovaries and placenta in females and by adrenal glands in both sexes. Progesterone is also synthesized by central nervous system (CNS) tissues to perform various vital neurological functions in the brain. Apart from performing crucial

Progesterone receptors: a key for neuroprotection in experimental stroke.

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Progesterone receptors (PR) are expressed throughout the brain. However, their functional significance remains understudied. Here we report a novel role of PR as crucial mediators of neuroprotection using a model of transient middle cerebral artery occlusion and PR knockout mice. Six hours after

Allopregnanolone and its precursor progesterone do not reduce injury after experimental stroke in hypertensive rats - role of postoperative temperature regulation?

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Allopregnanolone is a neurosteroid synthesized from progesterone in brain. It increases inhibition through modulation of the gamma-aminobutyric acid type A (GABA-A) receptor. Both agents are putative neuroprotectants after ischemic stroke. We sought to confirm their effectiveness in a hypertensive

Neuroprotective effects of progesterone following stroke in aged rats.

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Recent studies indicate that progesterone (PROG) protects against animal brain injury, including ischemic stroke, in various animal models. However, there are insufficient studies about PROG in other various groups such as ovariectomized females and aged animals. This study was designed to examine

Microglia and cyclooxygenase-2: possible therapeutic targets of progesterone for stroke.

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Previous studies have demonstrated that progesterone (PROG) may be a pleiotropic neuroprotective agent. Although there have been reports about the neurotoxicity of activated microglia and cyclooxygenase-2 (COX-2) in animal models of ischemic stroke, the influence of PROG on the activation of

Recombinant tissue plasminogen activator promotes, and progesterone attenuates, microglia/macrophage M1 polarization and recruitment of microglia after MCAO stroke in rats.

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BACKGROUND Tissue plasminogen activator (tPA) is one of the few approved treatments for stroke, but its effects on the phenotype of microglia/macrophages are poorly understood. One of its side effects is an increase in the inflammatory response leading to neuronal cell damage and death in the

Post-stroke infections exacerbate ischemic brain injury in middle-aged rats: immunomodulation and neuroprotection by progesterone.

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We investigated the effect of delayed, prolonged systemic inflammation on stroke outcomes and progesterone (P4) neuroprotection in middle-aged rats. After transient middle cerebral artery occlusion/reperfusion (MCAO) surgery, rats received P4 (8 or 16 mg/kg) or vehicle injections at 2h, 6h and every

Neuroprotection by progesterone after transient cerebral ischemia in stroke-prone spontaneously hypertensive rats.

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We investigated the neuroprotective effects of progesterone (P4) treatment in stroke-prone spontaneously hypertensive rats (SHRSPs) given 60-min transient middle cerebral artery occlusion (tMCAO). The treatment groups were: (1) Wistar-Kyoto (normotensive sham), (2) SHRSP (hypertensive sham), (3)

Progesterone exerts neuroprotective effects by inhibiting inflammatory response after stroke.

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OBJECTIVE We evaluated the inhibitory effects of progesterone (PROG) on inflammatory response and its influence on the structure of blood-brain barrier in a permanent model of stroke. METHODS One hundred and twenty adult male Sprague-Dawley rats were used in this study. METHODS PROG was dissolved in

Progesterone and allopregnanolone improves stroke outcome in male mice via distinct mechanisms but neither promotes neurogenesis.

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Based on the outcome of a number of experimental studies, progesterone (PROG) holds promise as a new therapy for stroke. To understand more about the mechanisms involved, we administered PROG (or the major metabolite, allopregnanolone, ALLO), intra-peritoneally, for a period of 24 h after transient

Progesterone in the treatment of neonatal arterial ischemic stroke and acute seizures: Role of BDNF/TrkB signaling.

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Neonatal stroke is among the top ten causes of childhood death and permanent disability in survivors, but no safe and effective acute treatments exist. To advance understanding of its neuroprotective mechanisms, we examined the effects of progesterone (PROG) on local and systemic inflammation

Is progesterone a candidate neuroprotective factor for treatment following ischemic stroke?

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Gender differences in stroke outcome have implicated steroid hormones as potential neuroprotective candidates. However, no clinical trials examining hormone replacement therapy on outcome following ischemic stroke have investigated the effect of progesterone-only treatment. In this review the

Progesterone Changes VEGF and BDNF Expression and Promotes Neurogenesis After Ischemic Stroke.

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Studies have shown that progesterone enhances functional recovery after ischemic stroke, but the underlying mechanisms are not completely understood. Therefore, we investigated the effect of progesterone on vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), and

Progesterone treatment for experimental stroke: an individual animal meta-analysis.

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Preclinical studies suggest progesterone is neuroprotective after cerebral ischemia. The gold standard for assessing intervention effects across studies within and between subgroups is to use meta-analysis based on individual animal data (IAD). Preclinical studies of progesterone in experimental

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