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Hazelnut-Derived Peptide YYLLVR Improves Endothelial Dysfunction in Hypertension by Activating ACE2.
Wentian Song1,2,3, Haoduo Huang1,2,3, Yue Shen3
1National Key Laboratory for Development and Utilization of Forest Food Resources, Zhejiang A&F University, Hangzhou, Zhejiang 311300, China.
Journal of Agricultural and Food Chemistry
|June 16, 2025
Summary
Hazelnut peptide YYLLVR effectively lowers blood pressure and improves endothelial function in hypertensive rats. This novel ACE2-activating peptide shows therapeutic potential for managing hypertension and related vascular dysfunction.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Pharmacology
Background:
- Hypertension and endothelial dysfunction are significant cardiovascular risk factors.
- The renin-angiotensin system (RAS) plays a crucial role in blood pressure regulation.
- Targeting the ACE2/Ang-(1-7)/MAS axis offers a potential therapeutic strategy for hypertension.
Purpose of the Study:
- To investigate the antihypertensive effects of YYLLVR, a hazelnut-derived peptide.
- To determine the impact of YYLLVR on endothelial dysfunction in spontaneously hypertensive rats (SHRs).
- To elucidate the molecular mechanisms underlying YYLLVR's action, focusing on the ACE/Ang II/AGTR1 and ACE2/Ang-(1-7)/MAS pathways.
Main Methods:
- Administration of YYLLVR to spontaneously hypertensive rats (SHRs).
- Measurement of systolic and diastolic blood pressure.
- Assessment of ACE2 expression and activity in vitro (HUVECs) and in vivo.
- Analysis of key molecular markers including nitric oxide (NO), eNOS, ET-1, iNOS, and inflammatory cytokines (IL-1β).
- Evaluation of endothelial cell apoptosis, tube formation, migration, and proliferation.
Main Results:
- YYLLVR significantly reduced systolic (53.48 mmHg) and diastolic (37.57 mmHg) blood pressure in SHRs.
- YYLLVR increased ACE2 expression (2-fold) and activity, promoting the ACE2/Ang-(1-7)/MAS axis while inhibiting the ACE/Ang II/AGTR1 axis.
- Enhanced NO and eNOS expression, reduced ET-1 and iNOS expression, and decreased aortic thickness were observed.
- YYLLVR demonstrated protective effects against Ang II-induced apoptosis and improved endothelial cell function.
- The effects of YYLLVR were dependent on ACE2 activity, as confirmed by experiments with an ACE2 inhibitor (DX600).
Conclusions:
- YYLLVR exhibits potent antihypertensive effects and improves endothelial dysfunction.
- Its mechanism involves the activation of the ACE2/Ang-(1-7)/MAS pathway and modulation of vascular inflammation and remodeling.
- YYLLVR represents a promising novel ACE2-activating peptide for the therapeutic management of hypertension and endothelial dysfunction.
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