Why the study?
Following the identification of an ACE inhibitory peptide (LPGP) from maize germ protein, the study aimed to explore its anti-vascular endothelial dysfunction effects and underlying mechanisms in Ang II-induced HUVECs.
The maize germ-derived ACE inhibitory peptide LPGP protects against Angiotensin II-induced endothelial dysfunction via the PI3K/Akt/eNOS pathway, suggesting potential anti-hypertensive properties.
LPGP attenuates Ang II-induced endothelial injury in vitro; hypothesis-generating for maize-derived peptides in vascular disease, with clinical relevance untested.
Our previous work identified an ACE inhibitory peptide (ACEIP) with a sequence of LPGP from maize germ protein. In this study, by employing Ang II-induced Human Umbilical Vein Endothelial Cells as a cell model, we aimed to explore the anti-vascular endothelial dysfunction (VED) effects of LPGP and its mechanisms of action. Our results elucidated that LPGP rescued the Ang II-induced cell injury by exerting cytoprotective effects, reducing apoptosis, relieving oxidative stress, and balancing the secretion of vasodilatory and vasoconstrictive factors. Moreover, we found that LPGP stimulated the expression of phosphorylated serine/threonine kinase B (p-Akt) and epithelial Nitric Oxide Synthase (p-eNOS). Finally, we proved that LPGP resists Ang II-induced injury through the PI3K/Akt/eNOS pathway. To our knowledge, we linked the VED repairing effects of a food-borne ACEIP to the PI3K/Akt/eNOS pathway for the first time, which opened a new avenue to verify and understand the potential anti-hypertension effects of food-derived ACEIPs.
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Li et al. (2023) studied this question.
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