RESUMO
CONTEXT: Docosahexaenoic acid (DHA) is one of the critical fatty acids for optimal health, which affect the expression of nerve growth factor and brain-derived neurotrophic factor in brain. OBJECTIVE: This study investigates whether DHA supplementation affects lipid peroxidation and activates the glial-derived neurotrophic factor (GDNF)-mitogen-activated protein kinase pathway (MAPK pathway) in hippocampus of natural aged rat. MATERIALS AND METHODS: Rats were randomly divided into four groups; DHA was orally administered at 80 and 160 mg/kg/day to 24-month female rats for 50 days. The antioxidant parameters and GDNF-GDNF family receptor α-1 (GFRα1)-tyrosine-protein kinase receptor (RET)-MAPK-cyclic AMP response element-binding protein (CERB) pathway were assayed in natural aged rat's hippocampus. RESULTS AND DISCUSSION: The results demonstrated that DHA supplementation significantly increased the activities of superoxide dismutase (SOD) by 37.39 and 57.69%, glutathione peroxidase (GSH-Px) by 27.62 and 32.57% decreased TBARS level by 28.49 and 49.05%, respectively, but did not significantly affect catalase (CAT), in hippocampus, when compared with the aged group. DHA supplementation in diet resulted in an increase of DHA level in hippocampus. Furthermore, we found that DHA supplementation markedly increased the levels of GDNF and GFRα1 and the phosphorylation of RET, and led to the activation of the MAPK pathway in hippocampus tissue. CONCLUSION: DHA supplementation can change fatty acids composition, improve antioxidant parameters and activate the GDNF-MAPK pathway in natural aged rat's hippocampus.
Assuntos
Envelhecimento/metabolismo , Suplementos Nutricionais , Ácidos Docosa-Hexaenoicos/uso terapêutico , Receptores de Fator Neurotrófico Derivado de Linhagem de Célula Glial/biossíntese , Fator Neurotrófico Derivado de Linhagem de Célula Glial/agonistas , Hipocampo/metabolismo , Fármacos Neuroprotetores/uso terapêutico , Animais , Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/agonistas , Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo , Ácidos Docosa-Hexaenoicos/administração & dosagem , Ácidos Docosa-Hexaenoicos/metabolismo , Feminino , Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo , Receptores de Fator Neurotrófico Derivado de Linhagem de Célula Glial/genética , Receptores de Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo , Hipocampo/enzimologia , Hipocampo/crescimento & desenvolvimento , Peroxidação de Lipídeos , Sistema de Sinalização das MAP Quinases , Proteínas do Tecido Nervoso/agonistas , Proteínas do Tecido Nervoso/metabolismo , Neurônios/enzimologia , Neurônios/metabolismo , Fármacos Neuroprotetores/administração & dosagem , Fármacos Neuroprotetores/metabolismo , Estresse Oxidativo , Oxirredutases/química , Oxirredutases/metabolismo , Fosforilação , Processamento de Proteína Pós-Traducional , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley , Regulação para CimaRESUMO
OBJECTIVE: To study the hypoglycemic effect and mechanism of the extracts of cactus pear fruit polysaccharide (CPFP) in diabetic rats induced by streptozotocin (STZ). METHODS: The diabetic rats were induced by STZ in SD rats, and randomly divided into model group, insulin group,cactus pear juice group, high dose CPFP group,low dose CPFP group. The experimental rats were administrated for 8 weeks. During the experiment, the contents of blood glucose and blood limit of the rats were detected and body weight were recorded. The pathology of beta cell and alpha cell in pancreas of experimental rats were observed by immunohistochemistry. RESULTS: Compared with model group, the contents of blood glucose, total cholesterol and triglyceride were remarkably decreased in high and low dose CPFP groups. At the same time the body weight was significantly increased in high dose and low dose CPFP groups. The results of immunohistochemical stain demonstrated that the number of islet beta cells was increased and that of islet alpha cells was unchanged in the treatment groups. CONCLUSION: CPFP can markedly decrease blood glucose and blood limit in STZ-induced diabetic rats. Its mechanism may be related to stimulating the secretion of insulin from beta cells.