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1.
Int J Mol Sci ; 11(10): 3988-98, 2010 Oct 19.
Artigo em Inglês | MEDLINE | ID: mdl-21152315

RESUMO

Lysophosphatidic acid (LPA), which is proposed to play an important role in normal physiological situations such as wound healing, vascular tone, vascular integrity and reproduction, may be involved in the etiology of some diseases such as atherosclerosis, cancer, obesity or myocardial infarction. Abnormal findings, including silent brain infarction (SBI), are frequently observed by magnetic resonance imaging (MRI) in patients with nonvalvular atrial fibrillation (NVAF). However, whether there is a relationship between LPA level and the prevalence of SBI has not been extensively studied. In the present study, the association between them was investigated. 235 patients with NVAF, 116 cases of SBI without NVAF and 120 cases of healthy volunteers (control group), who did not receive any antithrombotic therapy, were enrolled in this study. Plasma LPA levels in the NVAF with SBI group were significantly higher than that in the control group (p < 0.01), NVAF without SBI group (p < 0.01) and SBI without NVAF group (p < 0.01). The LPA levels are lower in the control group than in the NVAF without SBI and SBI without NVAF groups (p < 0.01), however, the latter two groups did not significantly differ from each other for LPA levels (p > 0.05) There were significant differences in the positive rate of platelet activation between each of the groups (p < 0.01). The positive rate of platelet activation was significantly higher in the NVAF with SBI group. We suggest that LPA might be a novel marker for estimation of the status of platelet activation and the risk factor for SBI onset in NVAF patients. We expected that plasma LPA levels could predict the occurrence of SBI in NVAF patients.


Assuntos
Fibrilação Atrial/sangue , Infarto Encefálico/diagnóstico , Lisofosfolipídeos/sangue , Idoso , Fibrilação Atrial/complicações , Fibrilação Atrial/diagnóstico , Biomarcadores/sangue , Infarto Encefálico/sangue , Infarto Encefálico/complicações , Estudos de Casos e Controles , Feminino , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Ativação Plaquetária
2.
Brain Res ; 1336: 58-65, 2010 Jun 08.
Artigo em Inglês | MEDLINE | ID: mdl-20399757

RESUMO

Increasing evidence suggests the beneficial effects of acupuncture on Parkinson's disease (PD). Although clinical evidence for the acupuncture anti-Parkinson's disease effect has been demonstrated, the precise mechanism still remains elusive. It has been suggested a relationship between PD and reactive oxygen species (ROS) can result in neurodegeneration. The aim of this study was to evaluate the status of oxidative stress, as well as the antioxidant enzyme response, and the role of acupuncture stimulation at GB34 (Yanglingquan), LR3 (Taichong), ST36 (Zusanli) and SP10 (Xuehai) acupoints on regulating oxidative stress in the nigrostriatal system in the 6-hydroxydopamine (6-OHDA) lesioned rat. Two weeks after unilateral injection of 6-OHDA into the left medial forebrain bundle (MFB), an apomorphine induced rotational behavior test was performed. The levels of enzymatic, viz., superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and nonenzymatic, viz., reduced glutathione (GSH), and the levels of malondialdehyde (MDA) in the nigrostriatal system were measured to assess the oxidative stress status. Brain MDA levels significantly increased, while GSH levels were decreased in impaired groups with 6-OHDA injection only, accompanied by a marked reduction in the level of SOD and GSH-Px. The levels of oxidative stress related parameters except CAT, as well as the rotational asymmetry, were reversed by acupuncture stimulation. These results showed that acupuncture treatment displayed antioxidative and/or neuroprotective properties in the 6-OHDA lesioned rat and these protective properties might be mediated, at least in part, by involving regulation of the antioxidant defense system.


Assuntos
Terapia por Acupuntura , Estresse Oxidativo/fisiologia , Transtornos Parkinsonianos/terapia , Adrenérgicos/toxicidade , Animais , Encéfalo/metabolismo , Química Encefálica/fisiologia , Catalase/metabolismo , Glutationa Peroxidase/metabolismo , Masculino , Malondialdeído/metabolismo , Oxidopamina/toxicidade , Transtornos Parkinsonianos/metabolismo , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismo
3.
Neurol Res ; 30(4): 366-9, 2008 May.
Artigo em Inglês | MEDLINE | ID: mdl-18544253

RESUMO

BACKGROUND AND PURPOSE: Lysophosphatidic acid (LPA) is released from activated platelets. Acetylsalicylate (aspirin) is the most commonly used antiplatelet drug. The purpose of this study is to observe whether treatment with acetylsalicylate decreases the LPA level in patients with ischemic cerebrovascular diseases. METHODS: We performed a study examining LPA level in fresh plasma in cases and controls enrolled in the LPA and Stroke Prevention Study. Level of LPA was assayed by measuring its inorganic phosphorus after separation by chromatography. RESULTS: An elevated LPA level was seen in cases (n = 254) with ischemic cerebrovascular disease (3.11+/- 1.55 micromol/l) compared with 136 healthy controls (1.77 +/- 1.04 micromol/l) (p < 0.001). Administration of aspirin (100 mg q.d.) for 1 month significantly lowered LPA level in patients (n = 142) (2.41 +/- 1.03 mu mol/l) compared with that before taking acetylsalicylate (4.06 +/- 1.03 micromol/l) (p < 0.001). However, the LPA level in patients (n = 36) who stopped acetylsalicylate after taking it for 1 month was re-elevated. Before and after taking acetylsalicylate for 1 month, their LPA levels were 4.23 +/- 1.15 and 1.93 +/- 0.85 micromol/l, respectively. After 1 month withdrawal, level was 3.90 +/- 1.09 micromol/l (p < 0.001 compared that before taking acetylsalicylate). CONCLUSION: Our findings support a close association between increased plasma LPA level and platelet activation. Acetylsalicylate could decrease plasma LPA levels, which may be used as a mechanism for acetylsalicylate in the prevention of ischemic stroke.


Assuntos
Aspirina/farmacologia , Plaquetas/efeitos dos fármacos , Isquemia Encefálica/sangue , Isquemia Encefálica/tratamento farmacológico , Lisofosfolipídeos/sangue , Aspirina/uso terapêutico , Biomarcadores/sangue , Plaquetas/metabolismo , Isquemia Encefálica/fisiopatologia , Regulação para Baixo/efeitos dos fármacos , Feminino , Humanos , Lisofosfolipídeos/biossíntese , Masculino , Pessoa de Meia-Idade , Fósforo/sangue , Inibidores da Agregação Plaquetária/farmacologia , Inibidores da Agregação Plaquetária/uso terapêutico , Resultado do Tratamento
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