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progesterone/atrophy
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Experimental and clinical evidence for the protective role of progesterone in motoneuron degeneration and neuroinflammation.
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Far beyond its role in reproduction, progesterone exerts neuro-protective, promyelinating, and anti-inflammatory effects in the nervous system. These effects are amplified under pathological conditions, implying that changes of the local environment sensitize nervous tissues to steroid therapy. The
Effects of testosterone, pregnenolone, progesterone and cortisol on pituitary and testicular function in male golden hamsters with gonadal atrophy induced by short photoperiods.
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Testicular regression was induced in adult golden hamsters by exposure to a short photoperiod (5 h light:19 h darkness). The response of these animals to exogenous steroids (ten injections each of 5 mg testosterone, testosterone propionate, pregnenolone, progesterone or cortisol administered s.c.
Effects of estradiol and progesterone on diabetes-associated utero-ovarian atrophy in C57BL/KsJ (db/db) mutant mice.
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The modulating effects of estradiol (E: 1 microgram/3.5 days) and progesterone (P: 2 mg/3.5 days) on the obesity and hyperinsulinemic and hyperglycemic components of the diabetes-obesity syndrome in female C57BL/KsJ (db/db) mice, which includes cellular atrophy and adiposity in the reproductive
Progesterone protects oocytes from premature degeneration within the follicle.
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The present study was designed to determine the effects of gestrinone (R2323) in the process of follicle rupture and oocyte maturation and degeneration in an in vitro perfused rabbit ovary model. In the first experiment, R2323 at 10(2), 10(3), or 10(4) ng/ml was added to the perfusate of one ovary.
Progesterone neuroprotection in traumatic CNS injury and motoneuron degeneration.
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Studies on the neuroprotective and promyelinating effects of progesterone in the nervous system are of great interest due to their potential clinical connotations. In peripheral neuropathies, progesterone and reduced derivatives promote remyelination, axonal regeneration and the recovery of
Ex Vivo Evaluation of Intravaginal Progesterone and Testosterone to Treat the Luteal-phase Deficiency and Vaginal Atrophy.
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The purpose of this study was to evaluate the transmucosal permeation of progesterone and testosterone using Pentravan as its vehicle for vaginal delivery. Progesterone deficiency is a hormone imbalance that could lead to luteal-phase deficiency, which is a common problem in assisted reproductive
Progesterone administration fails to protect albino male rats against photostress-induced retinal degeneration.
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OBJECTIVE
Female patients show better recovery after brain injury and lower incidence of vascular diseases before menopause. The aim of this study was to test the protective effect of female sexual hormones against photostress-induced photoreceptor apoptosis.
METHODS
Five week old male albino
Progesterone administration fails to protect albino male rats against photostress-induced retinal degeneration.
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OBJECTIVE
Female patients show better recovery after brain injury and lower incidence of vascular diseases before menopause. The aim of this study was to test the protective effect of female sexual hormones against photostress-induced photoreceptor apoptosis.
METHODS
Five week old male albino
Progesterone modulates brain-derived neurotrophic factor and choline acetyltransferase in degenerating Wobbler motoneurons.
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Progesterone (PROG) shows neuroprotective effects in nervous system diseases. The Wobbler mouse, a model of motoneuron degeneration, suffers a mutation of the Vsp154 gene on chromosome 11 leading to motoneuron vacuolation and astrocytosis of the spinal cord. Previous work has demonstrated beneficial
Stage dependent effects of progesterone on motoneurons and glial cells of wobbler mouse spinal cord degeneration.
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In the Wobbler mouse, a mutation in the Vps54 gene is accompanied by motoneuron degeneration and astrogliosis in the cervical spinal cord. Previous work has shown that these abnormalities are greatly attenuated by progesterone treatment of clinically afflicted Wobblers. However, whether progesterone
The progesterone receptor agonist Nestorone holds back proinflammatory mediators and neuropathology in the wobbler mouse model of motoneuron degeneration.
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Wobbler mutant mice suffer from progressive motoneuron degeneration and glial cell reactivity in the spinal cord. To prevent development of these abnormalities, we employed Nestorone, a high-affinity progesterone receptor agonist endowed with neuroprotective, promyelinating and anti-inflammatory
Comparative effects of progesterone and the synthetic progestin norethindrone on neuroprotection in a model of spontaneous motoneuron degeneration.
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The Wobbler mouse has been proposed as an experimental model of the sporadic form of amyotrophic lateral sclerosis (ALS). The administration of natural progesterone (PROG) to Wobbler mice attenuates neuropathology, inhibits oxidative stress, enhances the expression of genes involved in motoneuron
Association of luteal cell degeneration and progesterone deficiency with lysosomal storage disorder MLIV in Mcoln1-/- mouse model.
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TRPML1 (MCOLN1/Mcoln1) is a lysosomal counter ion channel. Mutations in MCOLN1 cause mucolipidosis type IV (MLIV), a progressive and severe lysosomal storage disorder with a slow onset. Mcoln1-/- mice recapitulate typical MLIV phenotypes but roles of TRPML1 in female reproduction are unknown.
Progesterone alleviates neural behavioral deficits and demyelination with reduced degeneration of oligodendroglial cells in cuprizone-induced mice.
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Demyelination occurs widely in neurodegenerative diseases. Progesterone has neuroprotective effects, is known to reduce the clinical scores and the inflammatory response. Progesterone also promotes remyelination in experimental autoimmune encephalomyelitis and cuprizone-induced demyelinating brain.
Progesterone Attenuates Microglial-Driven Retinal Degeneration and Stimulates Protective Fractalkine-CX3CR1 Signaling.
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Retinitis pigmentosa (RP) is a degenerative disease leading to photoreceptor cell loss. Mouse models of RP, such as the rd10 mouse (B6.CXBl-Pde6brd10/J), have enhanced our understanding of the disease, allowing for development of potential therapeutics. In 2011, our group first demonstrated that the
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