Proteoma miocárdico de ratos com disfunção cardíaca por estenose aórtica supravalvar atenuada pelo treinamento físico aeróbio
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Data
2021-09-02
Autores
Mota, Gustavo Augusto Ferreira
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Editor
Universidade Estadual Paulista (Unesp)
Resumo
Diferentes autores analisaram o efeito do treinamento físico (TFa) no coração patológico de roedores com estenose aórtica (EAo). Enquanto alguns autores não detectaram alteração no desempenho, outros mostraram que o TF promoveu atenuação da disfunção diastólica e/ou sistólica. Entretanto, estes trabalhos não analisaram os mecanismos envolvidos nos efeitos benéficos desta terapêutica. Desta forma, o objetivo deste estudo é investigar por meio do proteoma miocárdico os mecanismos envolvidos na atenuação da disfunção ventricular pelo TFa em ratos com EAo. Ratos Wistar foram divididos em quatro grupos: Sham, Sham exercitado (ShamTF), EAo e EAo exercitado (EAoTF). O TFa consistiu em cinco sessões de corrida, em esteira por semana, por 16 semanas. A análise estatística foi realizada por ANOVA ou teste de Kruskal-Wallis e teste de Goodman. Todos os resultados foram discutidos ao nível de significância de 5%. Ratos EAoTF apresentaram maior capacidade funcional, menor concentração de lactato sanguíneo, atenuação estrutural e funcional cardíaca quando comparados com o grupo EAo. A análise do proteoma miocárdico evidenciou aumento de proteínas relacionadas a via glicolítca, estresse oxidativo, inflamação e diminuição da beta-oxidação no grupo EAo vs Sham. O grupo EAoTF aumentou a expressão de uma proteína relacionada à biogênese mitocondrial e diminuiu proteínas intrincadas com o estresse oxidativo e inflamação. A avaliação das vias fisiológicas e patológicas hipertróficas por Western Blot, não mostrou diferença estatística entre os grupos avaliados, exceto para a p-p38, que aumentou no grupo EAo. Os dados proteômicos foram validados para proteínas relacionadas ao metabolismo lipídico e glicolítico. A análise do proteoma nos permitiu mostrar que o exercício físico atenua o estresse oxidativo, inflamação e acarreta melhoria no processo de biogênese mitocondrial. Os resultados encontrados nos fazem inferir que estes são os possíveis mecanismos relacionados com a cardioproteção gerada pelo treinamento físico aeróbio neste modelo de sobrecarga pressórica.
Different authors have analyzed the effect of physical training (ET) on the pathological heart of rodents with aortic stenosis (AS). While some authors did not detect changes in performance, others showed that ET promoted attenuation of diastolic and/or systolic dysfunction. However, these studies did not analyze the mechanisms involved in the beneficial effects of this therapy. Thus, the aim of this study is to investigate through myocardial proteome the mechanisms involved in the attenuation of ventricular dysfunction by ET in rats with AS. Wistar rats were divided into four groups: C-Sed, Control exercised (C-Ex), AS and AS exercised (AS-Ex). The ET consisted of five treadmill running sessions per week for 16 weeks. Statistical analysis was performed by ANOVA or Kruskal-Wallis test and Goodman test. All results were discussed at a significance level of 5%. AS-Ex rats had higher functional capacity, lower blood lactate concentration, structural and functional cardiac attenuation when compared to AS group. The myocardial proteome analysis showed an increase in proteins related to the glycolytic pathway, oxidative stress, inflammation and a decrease in beta-oxidation in AS vs C-Sed group. The AS-Ex group increased the expression of a protein related to mitochondrial biogenesis and decreased proteins intricate with oxidative stress and inflammation. The evaluation of physiological and pathological hypertrophic pathways by Western Blot did not show any statistical difference between the groups evaluated, except for p-p38, which increased in the AS group. Proteomic data were validated for proteins related to lipid and glycolytic metabolism. Proteome analysis allowed us to show that physical exercise attenuates oxidative stress, inflammation and improves the mitochondrial biogenesis process. The results found make us infer that these are the possible mechanisms related to the cardioprotection generated by physical training in this pressure overload model.
Different authors have analyzed the effect of physical training (ET) on the pathological heart of rodents with aortic stenosis (AS). While some authors did not detect changes in performance, others showed that ET promoted attenuation of diastolic and/or systolic dysfunction. However, these studies did not analyze the mechanisms involved in the beneficial effects of this therapy. Thus, the aim of this study is to investigate through myocardial proteome the mechanisms involved in the attenuation of ventricular dysfunction by ET in rats with AS. Wistar rats were divided into four groups: C-Sed, Control exercised (C-Ex), AS and AS exercised (AS-Ex). The ET consisted of five treadmill running sessions per week for 16 weeks. Statistical analysis was performed by ANOVA or Kruskal-Wallis test and Goodman test. All results were discussed at a significance level of 5%. AS-Ex rats had higher functional capacity, lower blood lactate concentration, structural and functional cardiac attenuation when compared to AS group. The myocardial proteome analysis showed an increase in proteins related to the glycolytic pathway, oxidative stress, inflammation and a decrease in beta-oxidation in AS vs C-Sed group. The AS-Ex group increased the expression of a protein related to mitochondrial biogenesis and decreased proteins intricate with oxidative stress and inflammation. The evaluation of physiological and pathological hypertrophic pathways by Western Blot did not show any statistical difference between the groups evaluated, except for p-p38, which increased in the AS group. Proteomic data were validated for proteins related to lipid and glycolytic metabolism. Proteome analysis allowed us to show that physical exercise attenuates oxidative stress, inflammation and improves the mitochondrial biogenesis process. The results found make us infer that these are the possible mechanisms related to the cardioprotection generated by physical training in this pressure overload model.
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Palavras-chave
Proteoma, Miocárdio, Disfunção ventricular, Treinamento físico aeróbio, Estenose aórtica supravalvar, Ratos, Proteome, Myocardium, Ventricular dysfunction, Aerobic exercise training, Supravalvular aortic stenosis, Rat