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1.
Food Chem ; 108(2): 533-41, 2008 May 15.
Artigo em Inglês | MEDLINE | ID: mdl-26059131

RESUMO

Galactose/glycine model systems of sugar concentration 0.035, 0.069, 0.139, and 0.278M were incubated at 60, 75, and 90°C separately for studying the reaction kinetics of color development, pH change, and system anti-oxidative activity change in Maillard reaction. The results indicated that system color development followed first-ordered kinetics on galactose concentration; system pH went linearly down with a logarithm-ordered kinetics on galactose concentration; and anti-oxidative activity reduced linearly with a first-ordered kinetics on galactose concentration. The values of Q10 and activation energy ranged from 1.98 to 2.00 and from 68.8 to 69.5kJ/mol, respectively, for these three properties.

2.
Artigo em Chinês | MEDLINE | ID: mdl-21180125

RESUMO

AIM: To study the effects of ginkgolides (Gin) on the expression of hypoxia-inducible factor-1alpha (H1F-1alpha) in primary cultured cortical neurons treated with CoCl2 and the relationship with ERK signal pathway. METHODS: We observed the effects of Gin (37.5 mg/L) on morphology and viability on primary cultured cortical neurons with treatment of CoCl2 (125 micromol/L). The expression of HIF-1alpha and p-ERK of neurons induced by CoCl2 pretreated with Gin were assessed by Western-blot. We analyzed the relationship between HIF-1alpha expression activated by Gin and ERK signal pathway with treatment of PD98059 (100 micromol/L), a selective inhibitor of ERK. RESULTS: It was shown that Gin had protective effects on CoCl2 damaged neurons by raising the neuronal viability. Some basic expression of HIF-1alpha and p-ERK were observed in normal cultured cortical neurons. The expression of HIF-1alpha and p-ERK increased strikingly when treated with CoCl2 for 4 h. The levels of HIF-1alpha and p-ERK increased even more in the neurons pretreated with Gin for 24 h before CoCl2. The levels of HIF-1alpha and p-ERK were notably inhibited with pretreatment of PD98059, while Gin could prevent this inhibition. CONCLUSION: Gin has protective effects on neurons damaged by CoCl2 which might be related to the increase of the level of HIF-1alpha and the activation of ERK signal pathway.


Assuntos
Ginkgolídeos/farmacologia , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Sistema de Sinalização das MAP Quinases , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Animais , Hipóxia Celular/efeitos dos fármacos , Células Cultivadas , Camundongos , Camundongos Endogâmicos ICR
3.
Space Med Med Eng (Beijing) ; 18(4): 303-5, 2005 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-16224855

RESUMO

OBJECTIVE: To observe the protective effects of Rhodiola-astragalus membranaceus mixture against brain damage during hypoxia under simulated plateau environment and the mechanisms maybe involved in. METHOD: Adult SD rats were randomly divided into 3 groups, which were normoxic control, simulated plateau hypoxia, and Rhodiola-astragalus membranaceus mixture pretreatment group. Rats in the latter two groups were exposed to simulated 8000 m altitude in a hypobaric chamber for 7 h. Water content, Na+, K(+)-ATPase activity and SOD activity in cerebral tissue, malondialdehyde (MDA) and lactic acid content in cerebral homogenate and serum were measured. RESULT: As compared with control group, cerebral water content was significantly higher in hypoxia group, while it was obviously lower in pretreatment group. MDA contents of hypoxia group both in cerebral homogenate and serum were higher than that of control group, while the pretreatment group they were both decreased obviously. Lactic acid content of hypoxia group in cerebral and in serum increased markedly and decreased drastically in pretreatment group compared to that of hypoxic group. CONCLUSION: Rhodiola-astragalus membranaceus mixture has preventive effects on hypoxic damage induced by simulated plateau environment. This prevention may be related to the antagonistic effect on membrane lipid peroxidation and the inhibition on the accumulation of lactic acid in brain tissue and serum.


Assuntos
Altitude , Astragalus propinquus , Medicamentos de Ervas Chinesas/farmacologia , Hipóxia Encefálica/prevenção & controle , Rhodiola , Adenosina Trifosfatases/efeitos dos fármacos , Adenosina Trifosfatases/metabolismo , Animais , Câmaras de Exposição Atmosférica , Proteínas de Transporte de Cátions , Líquido Extracelular/efeitos dos fármacos , Hipóxia Encefálica/tratamento farmacológico , Ácido Láctico/metabolismo , Malondialdeído/metabolismo , Fitoterapia , Ratos , Ratos Sprague-Dawley , Sódio/metabolismo , Superóxido Dismutase/efeitos dos fármacos , Superóxido Dismutase/metabolismo
4.
Artigo em Chinês | MEDLINE | ID: mdl-21158113

RESUMO

AIM: To study the effects of ginkgolides (Gin) on the expression of hypoxia inducible factor-1 (HIF-1alpha) in hypoxic/ischemic neurons. METHODS: The gene expression of HIF-1alpha pretreated with or without Gin (37.5 microg/ml) was observed by RT-PCR on primary cultured cortical neurons in the condition of hypoxia and oxygen-glucose deprivation. RESULTS: Some basic expression of HIF-1alpha mRNA were observed in cultured cortical neurons. The expression of HIF-1alpha mRNA increased after 24 h treatment with Gin. The level of HIF-la mRNA increased also after 1 h hypoxia and further enhanced after the pretreatment with Gin. The expression of HIF-1alpha mRNA decreased with the deprivation of both oxygen and glucose, which reversed after the pretreatment of Gin. CONCLUSION: Gin could increase the expression of HIF-1alpha mRNA in hypoxic/ischemic cortical neurons.


Assuntos
Ginkgolídeos/farmacologia , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Neurônios/metabolismo , Animais , Hipóxia Celular , Expressão Gênica , Subunidade alfa do Fator 1 Induzível por Hipóxia/genética , Camundongos , Camundongos Endogâmicos ICR , Neurônios/efeitos dos fármacos , RNA Mensageiro/genética
5.
Artigo em Chinês | MEDLINE | ID: mdl-21158118

RESUMO

AIM: To investigate the effect of Safflor yellow on the gene expression of neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) in neonatal asphyxia. METHODS: 30 minutes after SY 7 g/kg weight intraperitoneally was administered on the neonatal rats. After asphyxia for 40 minutes,the neonatal rats were reoxygenated for 48 h, and the nitric oxide synthases (NOSs) mRNA expression was assessed by semi-quantitative reverse transcription-polymerase chain reaction. RESULTS: Neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) were up in hypoxia/reoxygenation (H/R) 48 h group, while both of them were down significantly in SY group, but no change was observed on endothelial nitric oxide synthase (eNOS). CONCLUSION: The protective of SY from brain damage induced by neonatal asphyxia might be associated with expression of NOSs mRNA.


Assuntos
Encéfalo/metabolismo , Chalcona/análogos & derivados , Hipóxia/metabolismo , Óxido Nítrico Sintase Tipo III/metabolismo , Óxido Nítrico Sintase Tipo II/metabolismo , Óxido Nítrico Sintase Tipo I/metabolismo , Quinonas/farmacologia , Animais , Chalcona/farmacologia , Chalcona/uso terapêutico , Expressão Gênica , Hipóxia/prevenção & controle , Quinonas/uso terapêutico , RNA Mensageiro/genética , Ratos , Ratos Sprague-Dawley
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