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

IF 10.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Feiyan Yang , Zeyu He , Zhongxing Chu , Wen Li , Guangfan Qu , Han Lu , Yiping Tang , Shuguo Sun , Zhang Luo , Feijun Luo
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Abstract

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.

Abstract Image

Abstract Image

一种来自牦牛的活性肽可通过抑制血管内皮生长因子/MAPK/炎症信号传导抑制缺氧诱导的肺损伤。
肺血管重塑和炎症在缺氧诱发的肺部疾病中扮演着重要角色。我们之前的研究表明,牦牛奶渣肽可以缓解炎症。在本研究中,我们的结果表明,牦牛奶渣多肽(LV)对缺氧诱导的肺损伤动物模型的肺具有保护作用。灌胃牦牛奶肽能改善缺氧小鼠肺组织的肺血管重塑。代谢组学和转录组学的综合分析表明,5-KETE、8,9-EET和6-酮-前列腺素F1a可能是预防缺氧小鼠肺损伤的潜在靶点。这些代谢物可受 MAPK/VEGF 和炎症通路的调控。我们的数据表明,LV 可通过 Nrf2/NF-κB/MAPK/PHD-2 通路抑制细胞凋亡和炎症反应,保护缺氧诱导的肺上皮细胞损伤。综上所述,我们的研究结果表明,LV为预防缺氧诱导的肺损伤和炎症相关肺部疾病提供了新的治疗线索。
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来源期刊
Redox Biology
Redox Biology BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
19.90
自引率
3.50%
发文量
318
审稿时长
25 days
期刊介绍: Redox Biology is the official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe. It is also affiliated with the International Society for Free Radical Research (SFRRI). This journal serves as a platform for publishing pioneering research, innovative methods, and comprehensive review articles in the field of redox biology, encompassing both health and disease. Redox Biology welcomes various forms of contributions, including research articles (short or full communications), methods, mini-reviews, and commentaries. Through its diverse range of published content, Redox Biology aims to foster advancements and insights in the understanding of redox biology and its implications.
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