Your browser doesn't support javascript.
loading
Hydrogen-rich saline alleviates cardiomyocyte apoptosis by reducing expression of calpain1 via miR-124-3p.
Xue, Xiaofei; Xi, Wang; Li, Wei; Xiao, Jian; Wang, Zhinong; Zhang, Yufeng.
Afiliación
  • Xue X; Department of Cardiothoracic Surgery, Changzheng Hospital, Naval Military Medical University, 415 Fengyang Road, Shanghai, 200003, China.
  • Xi W; Department of Cardiothoracic Surgery, Changzheng Hospital, Naval Military Medical University, 415 Fengyang Road, Shanghai, 200003, China.
  • Li W; Department of Cardiothoracic Surgery, General Hospital of Central Theater Command, Wuhan, China.
  • Xiao J; Department of Cardiothoracic Surgery, Changzheng Hospital, Naval Military Medical University, 415 Fengyang Road, Shanghai, 200003, China.
  • Wang Z; Department of Cardiothoracic Surgery, Changzheng Hospital, Naval Military Medical University, 415 Fengyang Road, Shanghai, 200003, China.
  • Zhang Y; Department of Cardiothoracic Surgery, Changzheng Hospital, Naval Military Medical University, 415 Fengyang Road, Shanghai, 200003, China.
ESC Heart Fail ; 10(5): 3077-3090, 2023 10.
Article en En | MEDLINE | ID: mdl-37602925
AIMS: Molecular hydrogen has been exhibited a protective function in heart diseases. Our previous study demonstrated that hydrogen-rich saline (HRS) could scavenge free radicals selectively and alleviate the inflammatory response in the myocardial ischaemia/reperfusion (I/R) injury, but the underlying mechanism has not been fully clarified. METHODS AND RESULTS: Adult (10 weeks) C57BL/6 male mice and neonatal rat cardiomyocytes were used to establish I/R and hypoxia/reoxygenation (H/R) injury models. I/R and H/R models were treated with HRS to classify the mechanisms of cardioproctective function. In this study, we found that miR-124-3p was significantly decreased in both I/R and H/R models, while it was partially ameliorated by HRS pretreatment. HRS treatment also alleviated ischaemia-induced apoptotic cell death and increased cell viability during I/R process, whereas silencing expression of miR-124-3p abolished this protective effect. In addition, we identified calpain1 as a direct target of miR-124-3p, and up-regulation of miR-124-3 produced both activity and expression of calpain1. It was also found that compared with the HRS group, overexpression of calpain1 increased caspase-3 activities, promoted cleaved-caspase3 and Bax protein expressions, and correspondingly decreased Bcl-2, further reducing cell viability. These results illustrated that calpain1 overexpression attenuated protective effect of HRS on cardiomyocytes in H/R model. CONCLUSIONS: The present study showed a protective effect of HRS on I/R injury, which may be associated with miR-124-3p-calpain1 signalling pathway.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Calpaína / Daño por Reperfusión Miocárdica / MicroARNs Límite: Animals Idioma: En Revista: ESC Heart Fail Año: 2023 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Calpaína / Daño por Reperfusión Miocárdica / MicroARNs Límite: Animals Idioma: En Revista: ESC Heart Fail Año: 2023 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido