RESUMO
To examine the changes in erythropoietin (Epo) protein and its mRNA expression in rat brain subjected to focal ischemia and possible mechanism of the preconditioning of mitochondrial toxin 3-nitropropionic acid (3-NPA), rats were administrated either vehicle or 3-NPA at a dose of 20 mg/kg,intraperitoneally (ip), 3 days prior to a 2-h middle cerebral artery occlusion followed by 24- h reperfusion. Infarct volumes were measured by using 2, 3, 5 triphenylte trazolinm chloride (TTC)staining, and Epo protein and its mRNA levels were assessed by immunohistochemistry and reverse transcriptase polymerase chain reaction (RT-PCR), respectively. Our results showed that after reperfusion, Epo was found to be expressed extensively in the rat brain. It was most apparent in the basal nuclei and hippocampus, and was, to some extent, present in cortex. Preconditioning with 3-NPA caused a reduction in infarct volume. The expression of both Epo protein and mRNA increased significantly in the different brain areas in the 3-NPA pretreated group as compared with the non-pretreated ischemia model group. These results suggested that preconditioning with low dose 3-NPA could induce ischemic tolerance and neuro-protective effects by increasing the Epo expression in the ischemic and ischemia-related areas.
RESUMO
To examine the changes in erythropoietin (Epo) protein and its mRNA expression in rat brain subjected to focal ischemia and possible mechanism of the preconditioning of mitochondrial toxin 3-nitropropionic acid (3-NPA), rats were administrated either vehicle or 3-NPA at a dose of 20 mg/kg, intraperitoneally (ip), 3 days prior to a 2-h middle cerebral artery occlusion followed by 24-h reperfusion. Infarct volumes were measured by using 2, 3, 5 triphenylte trazolinm chloride (TTC) staining, and Epo protein and its mRNA levels were assessed by immunohistochemistry and reverse transcriptase polymerase chain reaction (RT-PCR), respectively. Our results showed that after reperfusion, Epo was found to be expressed extensively in the rat brain. It was most apparent in the basal nuclei and hippocampus, and was, to some extent, present in cortex. Preconditioning with 3-NPA caused a reduction in infarct volume. The expression of both Epo protein and mRNA increased significantly in the different brain areas in the 3-NPA pretreated group as compared with the non-pretreated ischemia model group. These results suggested that preconditioning with low dose 3-NPA could induce ischemic tolerance and neuro-protective effects by increasing the Epo expression in the ischemic and ischemia-related areas.
RESUMO
The involvement of apoptosis in mitochondrial toxin 3-nitropropionic acid (3-NPA)-induced ischemic tolerance to transient focal cerebral ischemia in rats and the mechanism was investigated. 3-NPA at a dose of 20 mg/kg or vehicle control was intraperitoneally into the rats. Three days later, rats were exposed to 2 h of middle cerebral artery occlusion followed by 24 h of reperfusion. Infarct volumes were assessed by 2,3,5-triphenyltetrazolinm chloride (TTC) staining 24 h after reperfusion. Neural cell apoptosis in cerebral ischemic penumbra was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) and flow cytometry methods (FCM). The results showed that as compared to the vehicle-treated group, pretreatment with 3-NPA could reduce the infarct volume by 23.3% and decrease the number of TUNEL-positive neural cells and apoptotic percentage by 47% (P<0.05) and 44.9% (P<0.01), respectively. It was concluded that the development of 3-NPA-induced ischemic tolerance in brain might be related to the decreases in neural cell apoptosis.
Assuntos
Animais , Masculino , Ratos , Apoptose , Córtex Cerebral , Circulação Cerebrovascular , Dano ao DNA , Infarto da Artéria Cerebral Média , Patologia , Ataque Isquêmico Transitório , Patologia , Precondicionamento Isquêmico , Artéria Cerebral Média , Patologia , Nitrocompostos , Propionatos , Traumatismo por Reperfusão , PatologiaRESUMO
AIM: To investigate the relationship between astroglial activation state and ischemic tolerance induced by low dose of 3 nitropropionic acid (3 NPA) in gerbil hippocampus. METHODS: Transient forebrain ischemic model was induced by bilateral common carotid arteries occlution. HE staining and immunohistochemistry were used to identify neuronal and astrocyte response. RESULTS: Preconditioning with 3 NPA produced protective effects of CA 1neurons. The number of glial fibrillary acidic protein positive astrocyte in hippocampal CA 1 region increased slightly in control group, but increased significantly in preconditioning of the brain with 3 nitropropionic acid. CONCLUSION: The state of astroglial activation is related to neuronal survival in ischemic tolerance induced by low dose of 3 nitropropionic acid.
RESUMO
Objective To investigate the involvement of Bcl-2 and Bax mRNA expressions in mitochondrial toxin 3-nitropropionic acid(3-NPA)induced ischemic tolerance to focal cerebral ischemia in rats.Methods Rats were administrated 3-NPA intraperitoneally at dose of 20 mg/kg 3 days prior to a 2 h middle cerebral artery occlusion followed by 1 h,6 h,12 h,24 h and 48 h of reperfusion.The Bcl-2 and Bax mRNA expressions were measured by reverse transcriptase polymerase chain reaction and compared to the sham operation group and ischemic reperfusion group.Results Compared to the sham operation group,the ischemic reperfusion and 3-NPA pretreated groups exhibited an increase in Bcl-2 and Bax mRNA after reperfusion every time point of focal cerebral ischemia(all(P