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Resveratrol protects against myocardial ischemic injury via the inhibition of NF-κB-dependent inflammation and the enhancement of antioxidant defenses

Resveratrol (RES) is a natural phenol which possesses multiple pharmacological actions. The present study aimed to determine whether RES protects against myocardial ischemic injury in association with the inhibition of NF-κB-dependent inflammation and the enhancement of antioxidant defenses in mice...

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Detalles Bibliográficos
Autores principales: He, Yuan, Lu, Xinlin, Chen, Tao, Yang, Yu, Zheng, Jing, Chen, Can, Zhang, Yuanqi, Lei, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7895514/
https://www.ncbi.nlm.nih.gov/pubmed/33537801
http://dx.doi.org/10.3892/ijmm.2021.4862
Descripción
Sumario:Resveratrol (RES) is a natural phenol which possesses multiple pharmacological actions. The present study aimed to determine whether RES protects against myocardial ischemic injury in association with the inhibition of NF-κB-dependent inflammation and the enhancement of antioxidant defenses in mice following acute myocardial infarction (AMI). Male C57/BL mice were randomly assigned to 3 groups as follows: The sham-operated (sham) group, AMI + vehicle group and AMI + RES group. Rat H9C2 cells were also used to examine the effects of RES on hypoxia-induced oxidative injury in vitro. Redox homeostasis in the mouse myocardium and rat H9C2 cells was determined post-treatment. The mRNA and protein levels of phosphorylated (p-)IκB kinase (p-IKK), p-nuclear factor (NF)-κB p65, interleukin (IL)-1β, IL-6, nerve growth factor (NGF) and insulin-like growth factor-1 (IGF-1) were measured by RT-qPCR and western blot analysis. It was found that RES slightly protected the myocardium against ischemic injury in mice, while it prevented the hypoxia-induced apoptosis of H9C2 cells. RES decreased the production of reactive oxygen species (ROS) and enhanced the activities of superoxide dismutase (SOD), glutathione (GSH) and glutathione peroxidase (GPx). RES also downregulated the protein and/or mRNA levels of p-IKK, p-NF-κB p65, IL-1β, IL-6, NGF and IGF-1 at 7 and 28 days after infarction. On the whole, these data indicate that RES protects the myocardium against ischemic injury in association with the inhibition of oxidative stress and inflammatory responses. Thus, RES has the potential to be used as an adjunctive therapeutic drug for heart diseases.