An active peptide from yak inhibits hypoxia-induced lung injury via suppressing VEGF/MAPK/inflammatory signaling

• Published in: Redox biology 2024-09, Vol.75, p.103252, Article 103252
• Main Authors: Yang, Feiyan, He, Zeyu, Chu, Zhongxing, Li, Wen, Qu, Guangfan, Lu, Han, Tang, Yiping, Sun, Shuguo, Luo, Zhang, Luo, Feijun
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis - drug effects; Cattle; Disease Models, Animal; Humans; Hypoxia; Hypoxia - drug therapy; Hypoxia - metabolism; Inflammation - drug therapy; Inflammation - metabolism; Lung injury; Lung Injury - drug therapy; Lung Injury - etiology; Lung Injury - metabolism; Lung Injury - pathology; Male; Metabolome; Mice; Peptide; Peptides - chemistry; Peptides - pharmacology; Peptides - therapeutic use; Pulmonary vascular remodeling; Research Paper; Signal Transduction - drug effects; Transcriptome; Vascular Endothelial Growth Factor A - genetics; Vascular Endothelial Growth Factor A - metabolism
• ISSN: 2213-2317; 2213-2317
• DOI: 10.1016/j.redox.2024.103252

Pulmonary vascular remodeling and inflammation play an important role in the hypoxic-induced lung diseases. Our previous investigations showed that peptide from yak milk residues could alleviate inflammation. In this study, our results suggest that peptide (LV) from yak milk residues peptide had protective effect of lung in the animal models of hypoxic-induced lung injury. LV Gavage could improve pulmonary vascular remodeling in the lung tissues of hypoxic mice. A comprehensive analysis of metabolomics and transcriptomics revealed that 5-KETE, 8,9-EET, and 6-keto-prostaglandin F1a might be potential targets to prevent lung injury in the hypoxic mice. These metabolites can be regulated by MAPK/VEGF and inflammatory pathways. Our data indicated that LV treatment could inhibit apoptosis and inflammation via Nrf2/NF-κB/MAPK/PHD-2 pathway and protected hypoxic-induced lung epithelial cells injury. Taken together, our results suggest that LV provides a novel therapeutic clue for the prevention of hypoxia-induced lung injury and inflammation-related lung diseases. [Display omitted]