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Microvasc Res ; 138: 104212, 2021 11.
Artigo em Inglês | MEDLINE | ID: mdl-34175330

RESUMO

BACKGROUND: The aim of this study was to investigate the effect of 8 weeks of aerobic exercise on the expression of mir-126 and some angiogenesis factors in the endothelial tissue of the cardiac muscle of type 2 diabetic rats. METHODS: Sixteen male Wistar rats were divided into two groups: diabetic control and diabetic training. Nicotinamide and streptozotocin injections were used to induce type 2 diabetes. After familiarization, the training group participated in an 8-week exercise protocol on a treadmill with an intensity of 25 m per minute, a slope of 5% and 30 min per session. RT-PCR was used to evaluate the expression of mir-126 and PI3K genes. Expression of raf1, VEGF, blood glucose and insulin was determined by ELISA and insulin resistance was assessed by HOMA-IR homeostasis model. Immunohistochemistry was used to measure the capillary density of the cardiac muscle. Data were analyzed by t-test for independent groups with a significance level of p < 0.05. RESULTS: Diabetes reduces angiogenesis in cardiac tissue, which is associated with a significant reduction in the expression of mir-126, raf1, VEGF and PI3K; while aerobic exercise increased the expression of mir-126, raf1, PI3K, VEGF. Exercise also decreased blood glucose levels and insulin resistance. CONCLUSION: It seems that aerobic exercise can prevent the destructive effects of diabetes by activating the angiogenic pathway of cardiac tissue. Therefore, regulatory processes through mir-126, which are influenced by aerobic exercise, can be a valuable strategy in developing new treatments for diabetes.


Assuntos
Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Tipo 2/metabolismo , Células Endoteliais/metabolismo , MicroRNAs/metabolismo , Miocárdio/metabolismo , Condicionamento Físico Animal , Esforço Físico , Animais , Glicemia/metabolismo , Diabetes Mellitus Experimental/genética , Diabetes Mellitus Experimental/fisiopatologia , Diabetes Mellitus Tipo 2/genética , Diabetes Mellitus Tipo 2/fisiopatologia , Regulação da Expressão Gênica , Resistência à Insulina , Masculino , MicroRNAs/genética , Fosfatidilinositol 3-Quinase/genética , Fosfatidilinositol 3-Quinase/metabolismo , Proteínas Proto-Oncogênicas c-raf/metabolismo , Ratos Wistar , Fator A de Crescimento do Endotélio Vascular/metabolismo
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