RESUMO
Reactive oxygen species (ROS) are highly reactive chemical species that may cause irreversible tissue damage, and play a critical role in cardiovascular diseases. Hydrogen sulfide (H2S) is a gasotransmitter that acts as a ROS scavenger with cardio-protective effects. In this study, we investigated the cytoprotective effect of H2S against H2O2-induced apoptosis in cardiomyocytes. H9c2 rat cardiomyoblasts were treated with H2S (100 µM) 24 h before challenging with H2O2 (100 µM). Apoptosis was then assessed by annexin V and PI, and mitochondrial membrane potential was measured using a fluorescent probe, JC-1. Our results revealed that H2S improved cell viability, reduced the apoptotic rate, and preserved mitochondrial membrane potential. An increased Bcl-2 to Bax ratio was also seen in myocytes treated with H2S after H2O2-induced stress. Our findings indicated a therapeutic potential for H2S in preventing myocyte death following ischemia/reperfusion.
Assuntos
Antioxidantes/farmacologia , Apoptose/efeitos dos fármacos , Peróxido de Hidrogênio , Sulfeto de Hidrogênio/farmacologia , Mioblastos Cardíacos/efeitos dos fármacos , Animais , Apoptose/fisiologia , Western Blotting , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Citometria de Fluxo/métodos , Potencial da Membrana Mitocondrial , Mioblastos Cardíacos/metabolismo , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Ratos , Espécies Reativas de Oxigênio/metabolismo , Valores de Referência , Reprodutibilidade dos Testes , Sulfetos/farmacologiaRESUMO
Reactive oxygen species (ROS) are highly reactive chemical species that may cause irreversible tissue damage, and play a critical role in cardiovascular diseases. Hydrogen sulfide (H2S) is a gasotransmitter that acts as a ROS scavenger with cardio-protective effects. In this study, we investigated the cytoprotective effect of H2S against H2O2-induced apoptosis in cardiomyocytes. H9c2 rat cardiomyoblasts were treated with H2S (100 μM) 24 h before challenging with H2O2 (100 μM). Apoptosis was then assessed by annexin V and PI, and mitochondrial membrane potential was measured using a fluorescent probe, JC-1. Our results revealed that H2S improved cell viability, reduced the apoptotic rate, and preserved mitochondrial membrane potential. An increased Bcl-2 to Bax ratio was also seen in myocytes treated with H2S after H2O2-induced stress. Our findings indicated a therapeutic potential for H2S in preventing myocyte death following ischemia/reperfusion.
Assuntos
Animais , Ratos , Apoptose/efeitos dos fármacos , Mioblastos Cardíacos/efeitos dos fármacos , Peróxido de Hidrogênio , Antioxidantes/farmacologia , Valores de Referência , Sulfetos/farmacologia , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Western Blotting , Reprodutibilidade dos Testes , Espécies Reativas de Oxigênio/metabolismo , Apoptose/fisiologia , Estresse Oxidativo/efeitos dos fármacos , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Mioblastos Cardíacos/metabolismo , Potencial da Membrana Mitocondrial , Citometria de Fluxo/métodos , Sulfeto de Hidrogênio/farmacologiaRESUMO
Extracellular exosomes are formed inside the cytoplasm of cells in compartments known as multivesicular bodies. Thus, exosomes contain cytoplasmic content. Multivesicular bodies fuse with the plasma membrane and release exosomes into the extracellular environment. Comprehensive research suggests that exosomes act as both inflammatory intermediaries and critical inducers of oxidative stress to drive progression of Alzheimer's disease. An important role of exosomes in Alzheimer's disease includes the formation of neurofibrillary tangles and beta-amyloid production, clearance, and accumulation. In addition, exosomes are involved in neuroinflammation and oxidative stress, which both act as triggers for beta-amyloid pathogenesis and tau hyperphosphorylation. Further, it has been shown that exosomes are strongly associated with beta-amyloid clearance. Thus, effective measures for regulating exosome metabolism may be novel drug targets for Alzheimer's disease.
