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1.
Cytokine ; 126: 154912, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31704480

RESUMO

Stem cell therapy is a promising strategy for recovering of injured cardiac tissue after acute myocardial infarction. The effects promoted by preventive physical training, beneficial for regeneration, are not yet understood on stem cell homing. In the present study, we evaluated the effect of preventive physical training on cell homing activation and associated mechanisms after acute myocardial infarction and therapy with adipose-derived stem cells in spontaneously hypertensive rats (SHR). Forty female SHR were allocated in sedentary (S), sedentary SHAM (S-SHAM), sedentary AMI (S-AMI), sedentary with cell therapy (S-ICT), aerobically trained (T), trained SHAM (T-SHAM), trained AMI (T-AMI) and trained with cell therapy (S-ICT) groups. Cell therapy was performed through the infusion of 2 × 105 ADSC/0.05 mL at the moment of AMI. Molecular markers of cell homing (SDF-1/CXCR4), inflammatory response (myeloperoxidase and cardiac expression of iNOS, gp91phox and NFkB), vasoconstrictor agents (Ang II and ET-1) and an angiogenesis inducer (VEGF) were measured. Functional capacity and echocardiographic parameters were also evaluated. Preventive physical training associated with cell therapy was able to reduce left ventricle ejection fraction losses in infarcted animals. Results demonstrated activation of the SDF-1/CXCR4 axis by physical training, besides a reduction in vasoconstrictor and systemic inflammatory responses. Physical training prior to AMI was able to induce a cardioprotective effect and optimize the reparative mechanism of cell therapy in an animal model of hypertension.


Assuntos
Quimiocina CXCL12/imunologia , Infarto do Miocárdio/fisiopatologia , Condicionamento Físico Animal/métodos , Receptores CXCR4/imunologia , Transplante de Células-Tronco , Vasoconstrição/fisiologia , Animais , Cardiotônicos , Ecocardiografia , Feminino , Hipertensão/fisiopatologia , Ratos , Ratos Endogâmicos SHR , Comportamento Sedentário , Volume Sistólico/fisiologia , Função Ventricular Esquerda/fisiologia
2.
Cardiovasc Ther ; 36(4): e12434, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29752864

RESUMO

AIM: To examine the interference of ß-blockers with the chemokine stromal cell-derived factor-1 (SDF-1) found in cell homing receptors, C-X-C chemokine receptor type 4 (CXCR-4) and CXCR-7, and regulatory proteins of homing pathways, we administered atenolol, carvedilol, metoprolol, and propranolol for 30 days using an orogastric tube to hypertensive rats. METHOD: We collected blood samples before and after treatment and quantified the levels of SDF-1 with enzyme-linked immunosorbent assay (ELISA). On day 30 of treatment, the spontaneously hypertensive rats (SHR) were euthanized, and heart, liver, lung, and kidney tissues were biopsied. Proteins were isolated for determining the expression of CXCR-4, CXCR-7, GRK-2 (G protein-coupled receptors kinase 2), ß-arrestins (ß1-AR and ß2-AR), and nuclear factor kappa B (NFκB). RESULTS: We found that the study drugs modulated these proteins, and metoprolol and propranolol strongly affected the expression of ß1-AR (P = .0102) and ß2-AR (P = .0034). CONCLUSION: ß-blockers modulated tissue expression of the proteins and their interactions following 30 days of treatment. It evidences that this class of drugs can interfere with proteins of cell homing pathways.


Assuntos
Antagonistas Adrenérgicos beta/farmacologia , Anti-Hipertensivos/farmacologia , Movimento Celular/efeitos dos fármacos , Hipertensão/tratamento farmacológico , Antagonistas de Receptores Adrenérgicos beta 1/farmacologia , Animais , Atenolol/farmacologia , Carbazóis/farmacologia , Carvedilol , Quimiocina CXCL12/sangue , Modelos Animais de Doenças , Quinase 2 de Receptor Acoplado a Proteína G/metabolismo , Hipertensão/sangue , Hipertensão/fisiopatologia , Rim/efeitos dos fármacos , Rim/metabolismo , Fígado/efeitos dos fármacos , Fígado/metabolismo , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Metoprolol/farmacologia , Miocárdio/metabolismo , NF-kappa B/metabolismo , Propanolaminas/farmacologia , Propranolol/farmacologia , Ratos Endogâmicos SHR , Receptores CXCR/metabolismo , Receptores CXCR4/metabolismo , Transdução de Sinais/efeitos dos fármacos , beta-Arrestina 1/metabolismo , beta-Arrestina 2/metabolismo
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