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Notch1-Nrf2 信号串扰通过减少 ROS 形成提供心肌保护。

Notch1-Nrf2 signaling crosstalk provides myocardial protection by reducing ROS formation.

机构信息

Department of Cardiac Surgery, The First Affiliated Hospital, Nanchang University, Nanchang, China.

Department of Obstetrics and Gynecology, Jiangxi Province hospital of integrated traditional Chinese and Western medicine, Nanchang, China.

出版信息

Biochem Cell Biol. 2020 Apr;98(2):106-111. doi: 10.1139/bcb-2018-0398. Epub 2020 Feb 18.

DOI:10.1139/bcb-2018-0398
PMID:32069075
Abstract

Both the Notch1 and Keap1-Nrf2 signaling pathways have cardioprotective effects, but the role of Notch1-Nrf2 crosstalk in myocardial ischemia-reperfusion injury is unclear. In this study, we established hypoxia-reoxygenation in neonate rat myocardial cells and employed γ-secretase inhibitor and curcumin to inhibit and activate the Notch1 and Keap1-Nrf2 signaling pathways, respectively. We found that the combined action of the Notch1 and Keap1-Nrf2 signaling pathways significantly increased cardiomyocyte viability, inhibited cardiomyocyte apoptosis, reduced the formation of reactive oxygen species, and increased antioxidant activities. In conclusion, these findings suggest that Notch1-Nrf2 crosstalk exerts myocardial protection by reducing the formation of reactive oxygen species.

摘要

Notch1 和 Keap1-Nrf2 信号通路均具有心脏保护作用,但 Notch1-Nrf2 串话在心肌缺血再灌注损伤中的作用尚不清楚。在这项研究中,我们建立了新生大鼠心肌细胞的缺氧-复氧模型,并分别使用 γ-分泌酶抑制剂和姜黄素来抑制和激活 Notch1 和 Keap1-Nrf2 信号通路。我们发现,Notch1 和 Keap1-Nrf2 信号通路的联合作用显著增加了心肌细胞活力,抑制了心肌细胞凋亡,减少了活性氧的形成,并增加了抗氧化活性。总之,这些发现表明 Notch1-Nrf2 串话通过减少活性氧的形成发挥心肌保护作用。

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