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1.
China Journal of Chinese Materia Medica ; (24): 1285-1289, 2013.
Artigo em Chinês | WPRIM | ID: wpr-294125

RESUMO

The purpose of the present study was to investigate the effects of icariin (ICA) on the content of beta-amyloid (Abeta) and the expression of neurotrophic factors in the brain of mitochondrial deficiency model rats. SD rats were infused subcutaneously with sodium azide, which is an inhibitor of mitochondrial respiratory chain complex IV, via a minipump (0. 5 mg . kg-1 h-1) for 28 days to establish the mitochondrial deficiency animal model. The activity of mitochondrial respiratory chain complex IV (i. e. cytochrome C oxidase, COX) in hippocampus was measured by biochemical methods. ELISA method was used to detect the content of Abeta in the brain. The expression of neurotrophic factors was detected by Western blot and immunohistochemistry methods. Image analysis was performed by Image-pro software. The results showed that chronic infusion of sodium azide by minipump induced a significant decrease in the activity of mitochondrial cytochrome C oxidase, an obvious increase in the content of Abeta, and a marked decline in the expression of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and its receptor TrkB in the brain of rats. Intragastrical administration of ICA (12 or 36 mg . kg-l) significantly ameliorated all these abnormalities in the model rats. In conclusion, ICA can increase mitochondrial activity, inhibit Abeta production, and enhance the expression of neurotrophic factors in the brain of model rats induced by sodium azide. The results suggested that ICA may have beneficial prospect for the treatment of Alzheimer's disease.


Assuntos
Animais , Ratos , Amiloide , Metabolismo , Encéfalo , Metabolismo , Fator Neurotrófico Derivado do Encéfalo , Metabolismo , Modelos Animais de Doenças , Ensaio de Imunoadsorção Enzimática , Flavonoides , Farmacologia , Usos Terapêuticos , Mitocôndrias , Metabolismo , Patologia , Doenças Mitocondriais , Tratamento Farmacológico , Metabolismo , Fator de Crescimento Neural , Metabolismo , Fatores de Crescimento Neural , Metabolismo , Ratos Sprague-Dawley , Receptor trkB , Metabolismo
2.
China Journal of Chinese Materia Medica ; (24): 2109-2112, 2008.
Artigo em Chinês | WPRIM | ID: wpr-283784

RESUMO

<p><b>OBJECTIVE</b>To investigate the effects of morroniside on H2O2-induced apoptosis in nerve cells.</p><p><b>METHOD</b>Human neuroblastoma cell line SH-SY5Y cells were pre-incubaed with morroniside (1, 10, and 100 micromol x L(-1)) for 24 h prior to exposure to H2O2 (500 micromol x L(-1)) for 18 h. The activity of reactive SOD was measured by a biochemical assay. The expression of caspase-3, caspase-9, Bcl-2 and Bax was determined by Wastern blotting method.</p><p><b>RESULT</b>Pretreatment of the cells with morroniside (10 and 100 micromol x L(-1)) increasd SOD activity by 14% (P<0.01) and 11% (P<0.05) in comparison with cells exposed only to H2O2. Morroniside (1, 10, 100 micromol x L(-1)) lowered caspase-3 level by 31% (P<0.01), 103% (P<0.001) and 95% (P<0.001), decreased caspase-9 content by 71% (P<0.001), 132% (P<0.001) and 37% (P<0.05), and increasd Bcl-1 level by 88% (P<0.01), 121% (P<0.001) and 60% (P<0.01) respectively but no significant change occurred in Bax level in comparison with cells exposed only to H2O2.</p><p><b>CONCLUSION</b>Morroniside has neuroprotection effect against H2O2-induced oxidation injury in nerve cell.</p>


Assuntos
Animais , Humanos , Camundongos , Apoptose , Western Blotting , Caspase 3 , Metabolismo , Caspase 9 , Metabolismo , Linhagem Celular Tumoral , Ativação Enzimática , Glicosídeos , Farmacologia , Peróxido de Hidrogênio , Farmacologia , Neurônios , Biologia Celular , Metabolismo , Oxidantes , Farmacologia , Proteínas Proto-Oncogênicas c-bcl-2 , Metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Superóxido Dismutase , Metabolismo
3.
China Journal of Chinese Materia Medica ; (24): 1667-1670, 2005.
Artigo em Chinês | WPRIM | ID: wpr-287350

RESUMO

<p><b>OBJECTIVE</b>To observe the change of nitric oxide (NO) and expression of nuclear factor-kappa B (NF-kappaB) in the cortex of cerebral infarction rat induced by photochemical reaction, and study the effect of extract from Cornus officinalis (whose main ingredient is iridoid glycoside) in the course of disease.</p><p><b>METHOD</b>After rats were fed with experimental drugs for 7 days, the model of cerebral infarction was induced. Spectrophotography and immunohistochemistry were used to detect the change of the content of NO, NOS and the expression of NF-kappaB in the cortex.</p><p><b>RESULT</b>Compared with control group, distinct infarction was visible in the model group, and the content of NO, the activity of NOS and the positive cell number of NF-kappaB were increased obviously. Compared with model group, the extract of C. officeinalis decreased the area of infarction, the content of NO, the activity of NOS and the positive cell number of NF-kappaB.</p><p><b>CONCLUSION</b>The iridoid glycoside of C. officinalis may have therapeutical effect on cerebral infarction through regulating the content of NO and NF-kappaB.</p>


Assuntos
Animais , Masculino , Ratos , Córtex Cerebral , Metabolismo , Patologia , Infarto Cerebral , Metabolismo , Patologia , Cornus , Química , Medicamentos de Ervas Chinesas , Farmacologia , NF-kappa B , Metabolismo , Óxido Nítrico , Metabolismo , Óxido Nítrico Sintase , Metabolismo , Plantas Medicinais , Química , Distribuição Aleatória , Ratos Sprague-Dawley
4.
Chinese Journal of Rehabilitation Theory and Practice ; (12): 38-40, 2004.
Artigo em Chinês | WPRIM | ID: wpr-977758

RESUMO

@#ObjectiveTo develop three animal models to mimic muscle tremors of Parkinson's disease and observe effects of Chinese herb compounds Jian-Xing on these models.MethodsPure muscle tremor mice models were developed by single intraperitoneal injection of arecoline or oxotremorine. The mitochondria damaged model was developed by intraperitoneal injection of MPTP(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) 20mg/kg for 8 days. Duration time of tremoring was recorded. The climbing time and spontaneous movements of MPTP mice were recorded. HPLC was used to detect the content of dopamine and it's metabolites in MPTP mice.ResultsAfter injection of oxotremorine or arecoline,model mice exhibited significant tremoring, duration time of tremor of mice in Jian-Xing group shortened significantly. As to MPTP model mice, climbing time of model mice prolonged, times of spontaneous movements of model mice decreased and the content of dopamine in striaturn decreased compared with control group. Climbing time of mice in Jian-Xing group shortened, spontaneous movements increased and content of dopamine increased distinctively. ConclusionOxotremorine, arecoline and MPTP all can produce tremor animal models. Chinese herb compounds Jian-Xing can shorten the duration time of tremor.As to MPTP model, Jian-Xing can shorten the climbing time of model mice, increase the spontaneous movements and increase the content of dopamine in striaturn.

5.
Acta Nutrimenta Sinica ; (6)1956.
Artigo em Chinês | WPRIM | ID: wpr-679192

RESUMO

Objective: To investigate the effect of taurine on learning and memory impairment, cytokines secretion in rats intrahippocampally injected with ?-amyloid (A?) 1-40. Methods: SD rats were randomly divided into control group, A? injected group, taurine (0.3g/kg?d, 0.6g/kg?d) groups. The rats were fed with taurine for 7 days, and then subjected to bilateral intrahippocampus injection of A?1-40 or vehicle. Two weeks later, all rats performed Morris water maze test. The contents of IL-6, TNF-? were checked by way of radio-immunity assay for hippocampus samples. Results: Compared with A?model group, the escape latency and distance were significantly reduced in taurine (0.6g/kg?d) group; the ratio of swimming distance in the target quadrant to that in the whole pool of the probe trial; the content of cytokines of IL-6 and TNF-?in hippocampus were reduced significantly. Conclusion: Taurine can effectively attenuate the cognitive dysfunction caused by A?1-40 in rats. The reduced cytokines content in hippocampus might contribute to this effect.

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