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Article Publish Status: FREE
Abstract Title:

Naringenin ameliorates homocysteine induced endothelial damage via the AMPKα/Sirt1 pathway.

Abstract Source:

J Adv Res. 2021 Dec ;34:137-147. Epub 2021 Jan 23. PMID: 35024186

Abstract Author(s):

Hui Li, Linlin Liu, Zhiwen Cao, Wen Li, Rui Liu, Youwen Chen, Chenxi Li, Yurong Song, Guangzhi Liu, Jinghong Hu, Zhenli Liu, Cheng Lu, Yuanyan Liu

Article Affiliation:

Hui Li

Abstract:

Introduction: Endothelial damage (ED) has been implicated in accelerating the development of atherosclerosis. The latter condition is a risk factor for developing several cardiovascular diseases (CVDs) associated with high morbidity and mortality rates worldwide.

Objectives: In our previous studies, we found naringenin (Nar), a bioactive flavanone compound, to protect against mitochondrial damage and oxidative stress. Though the pleiotropic effects of Nar have been well described, precise cytoprotective mechanisms of Nar against homocysteine (Hcy) induced ED remains elusive. Understanding these events may give an insight in to prevention and treatment of CVDs.

Methods: After ruling out the NMDA-R1 mediated pathway, RNA-Seq, a novel transcriptomic technique uncovered AMPK signaling pathway was identified as the mechanism with which Nar corrects ED. Further in vivo and in vitro tests validated the role of Nar against ED.

Results: In particular, Nar activates AMPKα/Sirt1 signaling pathway, which restores mitochondrial Cabalance and ultimately lowered production of reactive oxygen species (ROS). Activated AMPKα/Sirt1 signaling pathway also up-regulates endothelial nitric oxide synthase (eNOS) activity, and then increasing the production of nitric oxide (NO), ultimately ameliorating ED.

Conclusion: Nar could increase the ROS elimination and decrease eNOS uncoupling, subsequently upregulate the NO bioavailability and endothelial function by activating AMPKα/Sirt1 signaling pathway.

Study Type : In Vitro Study

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