| Literature DB >> 27667182 |
Lei Yang1, Yan Zhang2, Mengmeng Zhu2, Qiong Zhang3, Xiaoling Wang2, Yanjiao Wang2, Jincai Zhang2, Jing Li2, Liang Yang2, Jie Liu2, Fei Liu2, Yinan Yang2, Licheng Kang2, Yanna Shen4, Zhi Qi5.
Abstract
The objective was to examine the protective effect of resveratrol (RSV) on myocardial ischemia/reperfusion (IR) injury and whether the mechanism was related to vascular endothelial growth factor B (VEGF-B) signaling pathway. Rat hearts were isolated for Langendorff perfusion test and H9c2 cells were used for in vitro assessments. RSV treatment significantly improved left ventricular function, inhibited CK-MB release, and reduced infarct size in comparison with IR group ex vivo. RSV treatment markedly decreased cell death and apoptosis of H9c2 cells during IR. We found that RSV was responsible for the up-regulation of VEGF-B mRNA and protein level, which caused the activation of Akt and the inhibition of GSK3β. Additionally, RSV prevented the generation of reactive oxygen species (ROS) by up-regulating the expression of MnSOD either in vitro or ex vivo. We also found that the inhibition of VEGF-B abolished the cardioprotective effect of RSV, increased apoptosis, and led to the down-regulation of phosphorylated Akt, GSK3β, and MnSOD in H9c2 cells. These results demonstrated that RSV was able to attenuate myocardial IR injury via promotion of VEGF-B/antioxidant signaling pathway. Therefore, the up-regulation of VEGF-B can be a promising modality for clinical myocardial IR injury therapy.Entities:
Keywords: Apoptosis; Myocardial ischemia reperfusion injury; ROS; Resveratrol; VEGF-B
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Year: 2016 PMID: 27667182 DOI: 10.1016/j.freeradbiomed.2016.09.016
Source DB: PubMed Journal: Free Radic Biol Med ISSN: 0891-5849 Impact factor: 7.376