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1.
J Integr Neurosci ; 16(4): 385-400, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28891528

RESUMO

Alzheimer's Disease (AD) is one of the commonest neural degeneration in aging population, and has become a global health challenge. 2-(2-benzofuranyl)-2-imidazoline (2-BFI) was reported to effectively improved the damage of patients with neuropathological disorders. In the present study, we investigated the effect of 2-BFI on the improvement of antioxidative, inflammation, and apoptosis in AD rats. Sprague-Dawley rats (2 months old, n=40) were used in this study and after injection of Aß1-42 into hippocampal CA1 (Cornu Ammonis) region, the rats were given high, moderate and low dose of 2-BFI though intraperitoneal (i.p.) injection. Then spatial memory and navigation ability were analyzed by Morrize Water Maze. For the molecular testing, chemical colorimetry, ELISA and immunoblotting were performed to measure the activities of antioxidative enzymes, the abundance of immune cytokines and expression of apoptotic proteins, respectively. Hematoxylin and Eosin staining was used to analyze the pathological changes. We observed that 2-BFI significantly ameliorated the learning and memory abilities in rat models with AD by dosage treatment, as demonstrated by the shorten learning latency and greater times of travel across the platform quadrant. Additionally, reactive oxygen species (ROS) and malondialdehyde (MDA), were decreased after treatment of 2-BFI with dosage dependency, while the activities of superoxidase dismutase (SOD) and (GPX) Glutathione peroxidase were in turn enhanced, suggesting that 2-BFI could protect the antioxidative enzymes and reduce the oxidative stress in the hippocampus. Moreover, the expression of inflammatory factors including TNF-a and IL-1ß were decreased after 2-BFI treatment. Additionally, the neuronal apoptosis was also attenuated, as shown by Western blot results. Taken together, the cognitive impairment in AD rats could be significantly improved by 2-BFI in a dose-dependent manner through suppressing oxidants accumulation, inhibiting of inflammatory response, as well as enhancing the neural viability.


Assuntos
Doença de Alzheimer/tratamento farmacológico , Apoptose/efeitos dos fármacos , Benzofuranos/farmacologia , Imidazóis/farmacologia , Inflamação/tratamento farmacológico , Fármacos Neuroprotetores/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Doença de Alzheimer/patologia , Doença de Alzheimer/fisiopatologia , Peptídeos beta-Amiloides , Animais , Anti-Inflamatórios não Esteroides/farmacologia , Apoptose/fisiologia , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Hipocampo/patologia , Inflamação/patologia , Inflamação/fisiopatologia , Aprendizagem em Labirinto/efeitos dos fármacos , Aprendizagem em Labirinto/fisiologia , Nootrópicos/farmacologia , Estresse Oxidativo/fisiologia , Fragmentos de Peptídeos , Distribuição Aleatória , Ratos Sprague-Dawley , Memória Espacial/efeitos dos fármacos , Memória Espacial/fisiologia , Navegação Espacial/efeitos dos fármacos , Navegação Espacial/fisiologia
2.
Inflammation ; 40(4): 1123-1130, 2017 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-28405851

RESUMO

Fluoride is a common element in nature and our daily life, and excessive intake of this element can cause fluorosis and irreversible brain damage. The toxic effects of fluoride on the central nervous system may be attributed to the release of inflammatory cytokines and ROS. GSK3ß is a key protein that modulates NF-κB activity and inflammatory cytokine levels and plays an important role in the Wnt signaling pathway. In this study, we found that fluoride altered the inflammatory status and oxidative stress by inhibiting Wnt signaling pathway activity. This study thus provides a valid basis for the fluorine-induced neuroinflammation injury theory.


Assuntos
Fluoretos/efeitos adversos , Inflamação/induzido quimicamente , Microglia/patologia , Via de Sinalização Wnt/efeitos dos fármacos , Linhagem Celular , Sistema Nervoso Central/patologia , Citocinas/metabolismo , Humanos , Microglia/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo
3.
J Ethnopharmacol ; 140(2): 339-44, 2012 Mar 27.
Artigo em Inglês | MEDLINE | ID: mdl-22306289

RESUMO

ETHNOPHARMACOLOGICAL RELEVANCE: Buyang Huanwu Decoction, a traditional Chinese medicine, consists of different herbal medicines, and has been traditionally used for centuries to treat paralysis and stroke. However, its optimal therapeutic time window and the mechanism are still unclear. AIM OF THE STUDY: This study was designed to explore the therapeutic time window and mechanism of Buyang Huanwu Decoction on transient focal cerebral ischemia/reperfusion injury. MATERIALS AND METHODS: Middle cerebral artery occlusion was conducted in male Sprague-Dawley rats, and 40g/kg of Buyang Huanwu Decoction was intragastrically infused at different time points, and the same dose was infused every 24h for 3 days. The level of glutamate in cerebrospinal fluid and the expression of metabotropic glutamate receptor-1 RNA in striatum were detected before, during, and after ischemia/reperfusion. Neurological deficit scores and brain infarction volumes were measured at 72h after reperfusion. RESULT: Cerebral ischemia/reperfusion resulted in significant neurological deficit and extensive cerebral infarct volume, associated with a large amount of glutamate in cerebrospinal fluid and elevation of metabotropic glutamate receptor-1 RNA expression. Buyang Huanwu Decoction significantly suppressed the release of glutamate, and reduced the expression of metabotropic glutamate receptor-1 RNA. The neurological defect score and infarction volume were significantly improved by administration of Buyang Huanwu Decoction, when compared with the Ischemia group. CONCLUSIONS: Administration of Buyang Huanwu Decoction, within 4h of post-transient focal stroke, reduced significant cerebral ischemia/reperfusion damage. The neuroprotective mechanism of Buyang Huanwu Decoction is, in part, associated with the down-regulation of metabotropic glutamate receptor-1 RNA and inhibition of glutamate release resulting from cerebral ischemia.


Assuntos
Medicamentos de Ervas Chinesas/farmacologia , Ácido Glutâmico/líquido cefalorraquidiano , Ataque Isquêmico Transitório/tratamento farmacológico , Magnoliopsida , Fármacos Neuroprotetores/farmacologia , Traumatismo por Reperfusão/prevenção & controle , Acidente Vascular Cerebral/tratamento farmacológico , Animais , Infarto Cerebral/prevenção & controle , Transtornos Cerebrovasculares , Medicamentos de Ervas Chinesas/uso terapêutico , Ataque Isquêmico Transitório/metabolismo , Masculino , Doenças do Sistema Nervoso/prevenção & controle , Fármacos Neuroprotetores/uso terapêutico , Oligoquetos , Fitoterapia , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Receptores de Glutamato Metabotrópico/genética , Receptores de Glutamato Metabotrópico/metabolismo , Traumatismo por Reperfusão/metabolismo , Acidente Vascular Cerebral/metabolismo , Fatores de Tempo
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