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

被引:15
|
作者
He, Yuan [1 ]
Lu, Xinlin [2 ]
Chen, Tao [2 ]
Yang, Yu [3 ]
Zheng, Jing [4 ]
Chen, Can [2 ]
Zhang, Yuanqi [5 ]
Lei, Wei [1 ,2 ]
机构
[1] Guangdong Med Univ, Affiliated Hosp, Lab Cardiovasc Dis, 57 South Renmin Ave, Zhanjiang 524001, Guangdong, Peoples R China
[2] Guangdong Med Univ, Affiliated Hosp, Cardiovasc Med Ctr, 57 South Renmin Ave, Zhanjiang 524001, Guangdong, Peoples R China
[3] Guangdong Med Univ, Affiliated Hosp, Gerontol Ctr, Zhanjiang 524001, Guangdong, Peoples R China
[4] Univ Wisconsin, Dept Obstet & Gynecol, Madison, WI 53715 USA
[5] Guangdong Med Coll, Affiliated Hosp, Dept Vasc Thyroid & Breast Surg, Zhanjiang 524001, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
resveratrol; myocardial ischemic injury; oxidative stress; inflammation; NF-κ B; OXIDATIVE STRESS; GENE-EXPRESSION; RAT-HEART; REPERFUSION;
D O I
10.3892/ijmm.2021.4862
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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-kappa B-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-)I kappa B kinase (p-IKK), p-nuclear factor (NF)-kappa B p65, interleukin (IL)-1 beta, 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-kappa B p65, IL-1 beta, 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.
引用
收藏
页数:12
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