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[Display omitted] • LPGP counteracted the Ang II-induced vascular endothelial dysfunction of HUVECs. • LPGP balanced the secretion of vasodilatory and vasoconstrictive factors in HUVECs. • LPGP activated the PI3K/Akt/eNOS pathway in HUVECs. • LPGP conferred its VED repairing function through the PI3K/Akt/eNOS pathway. • LPGP could serve as a potential anti-hypertension food ingredient. 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. [ABSTRACT FROM AUTHOR]