Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 4 de 4
Filtrar
Mais filtros











Intervalo de ano de publicação
1.
Mol Neurobiol ; 55(7): 6155-6168, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29250715

RESUMO

Although training programs with regular eccentric (ECC) exercise are more commonly used for improving muscular strength and mobility, ECC exercise effects upon functional recovery of the sciatic nerve has not yet been determined. After sciatic nerve crush, different mice groups were subjected to run on the treadmill for 30 min at a speed of 6, 10, or 14 m/min with - 16° slope, 5 days per week, over 8 weeks. During the training time, neuropathic pain-like behavior (mechanical and cold hyperalgesia) was assessed and functional recovery was determined with the grip strength test and the Sciatic Functional and Static indexes (SFI and SSI). After 9 weeks, triceps surae muscle weight and morphological alterations were assessed. Tumor necrosis factor alpha (TNF-α), interleukin-1ß (IL-1ß), interleukin-4 (IL-4), interleukin-1Ra (IL-1Ra), insulin-like growth factor-1 (IGF-1) levels, and markers pro- and anti-inflammatory and regeneration, respectively, were quantified in the muscle and sciatic nerve on day 14 post-crushing. Exercised groups presented less neuropathic pain-like behavior and better functional recovery than non-exercised groups. Biochemically, ECC exercise reduced TNF-α increase in the muscle. ECC exercise increased sciatic nerve IGF-1 levels in sciatic nerve crush-subjected animals. These findings provide new evidence indicating that treatment with ECC might be a potential approach for neuropathy induced by peripheral nerve injury.


Assuntos
Comportamento Animal , Fator de Crescimento Insulin-Like I/metabolismo , Atividade Motora , Neuralgia/patologia , Neuralgia/fisiopatologia , Condicionamento Físico Animal , Recuperação de Função Fisiológica , Traumatismos do Sistema Nervoso/fisiopatologia , Animais , Citocinas/metabolismo , Hiperalgesia/metabolismo , Hiperalgesia/patologia , Hiperalgesia/fisiopatologia , Mediadores da Inflamação/metabolismo , Masculino , Regeneração Nervosa , Neuralgia/metabolismo , Nervo Isquiático/lesões , Nervo Isquiático/patologia , Fatores de Tempo , Traumatismos do Sistema Nervoso/metabolismo , Traumatismos do Sistema Nervoso/patologia
2.
PLoS One ; 11(3): e0151855, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-26998608

RESUMO

BACKGROUND: The human T-Cell Lymphotropic Virus Type 1 (HTLV-1) is a retrovirus associated with neurological alterations; individuals with HTLV-1 infection may develop HTLV-1 associated myelopathy / tropical spastic paraparesis (HAM/TSP). Frequent neurological complaints include foot numbness and leg weakness. In this study, we compared the distribution of the body weight on different areas of the foot in HTLV-1 patients with HAM/TSP, asymptomatic HTLV-1 patients, and healthy individuals. METHODOLOGY: We studied 36 HTLV-1 infected patients, who were divided in two groups of 18 patients each based on whether or not they had been diagnosed with HAM/TSP, and 17 control subjects. The evaluation included an interview on the patient's clinical history and examinations of the patient's reflexes, foot skin tactile sensitivity, and risk of falling. The pressure distribution on different areas of the foot was measured with baropodometry, using a pressure platform, while the patients had their eyes open or closed. MAIN FINDINGS: The prevalence of neurological disturbances-altered reflexes and skin tactile sensitivity and increased risk of falling-was higher in HTLV-1 HAM/TSP patients than in HTLV-1 asymptomatic patients. The medium and maximum pressure values were higher in the forefoot than in the midfoot and hindfoot in both HTLV-1 groups. In addition, the pressure on the hindfoot was lower in HAM/TSP patients compared to control subjects. CONCLUSIONS: The neurological disturbances associated with HTLV-1 infection gradually worsened from HTLV-1 asymptomatic patients to HAM/TSP patients. Baropodometry is a valuable tool to establish the extent of neurological damage in patients suffering from HTLV-1 infection.


Assuntos
Pé/fisiopatologia , Infecções por HTLV-I/fisiopatologia , Infecções por HTLV-I/virologia , Vírus Linfotrópico T Tipo 1 Humano/fisiologia , Pressão , Traumatismos do Sistema Nervoso/fisiopatologia , Traumatismos do Sistema Nervoso/virologia , Adulto , Feminino , Infecções por HTLV-I/complicações , Humanos , Masculino , Pessoa de Meia-Idade , Traumatismos do Sistema Nervoso/complicações , Traumatismos do Sistema Nervoso/patologia
3.
Front Neuroendocrinol ; 30(2): 173-87, 2009 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-19318112

RESUMO

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 function. In traumatic brain injury (TBI), progesterone has the ability to reduce edema and inflammatory cytokines, prevent neuronal loss and improve functional outcomes. Clinical trials have shown that short-and long-term progesterone treatment induces a significant improvement in the level of disability among patients with brain injury. In experimental spinal cord injury (SCI), molecular markers of functional motoneurons become impaired, including brain-derived neurotrophic factor (BDNF) mRNA, Na,K-ATPase mRNA, microtubule-associated protein 2 and choline acetyltransferase (ChAT). SCI also produces motoneuron chromatolysis. Progesterone treatment restores the expression of these molecules while chromatolysis subsided. SCI also causes oligodendrocyte loss and demyelination. In this case, a short progesterone treatment enhances proliferation and differentiation of oligodendrocyte progenitors into mature myelin-producing cells, whereas prolonged treatment increases a transcription factor (Olig1) needed to repair injury-induced demyelination. Progesterone neuroprotection has also been shown in motoneuron neurodegeneration. In Wobbler mice spinal cord, progesterone reverses the impaired expression of BDNF, ChAT and Na,K-ATPase, prevents vacuolar motoneuron degeneration and the development of mitochondrial abnormalities, while functionally increases muscle strength and the survival of Wobbler mice. Multiple mechanisms contribute to these progesterone effects, and the role played by classical nuclear receptors, extra nuclear receptors, membrane receptors, and the reduced metabolites of progesterone in neuroprotection and myelin formation remain an exciting field worth of exploration.


Assuntos
Neurônios Motores/efeitos dos fármacos , Neurônios Motores/patologia , Degeneração Neural , Fármacos Neuroprotetores , Traumatismos do Sistema Nervoso , Animais , Lesões Encefálicas/tratamento farmacológico , Lesões Encefálicas/patologia , Lesões Encefálicas/fisiopatologia , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Ensaios Clínicos como Assunto , Modelos Animais de Doenças , Humanos , Camundongos , Camundongos Mutantes Neurológicos , Neurônios Motores/citologia , Neurônios Motores/metabolismo , Bainha de Mielina/metabolismo , Degeneração Neural/tratamento farmacológico , Degeneração Neural/patologia , Degeneração Neural/fisiopatologia , Fármacos Neuroprotetores/farmacologia , Fármacos Neuroprotetores/uso terapêutico , Oligodendroglia/citologia , Oligodendroglia/efeitos dos fármacos , Oligodendroglia/metabolismo , Receptores de Progesterona/metabolismo , Fatores Sexuais , Traumatismos da Medula Espinal/tratamento farmacológico , Traumatismos da Medula Espinal/patologia , Traumatismos da Medula Espinal/fisiopatologia , Traumatismos do Sistema Nervoso/tratamento farmacológico , Traumatismos do Sistema Nervoso/patologia , Traumatismos do Sistema Nervoso/fisiopatologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA