A peptide from yak ameliorates hypoxia-induced kidney injury by inhibiting inflammation and apoptosis via Nrf2 pathway

• Published in: Food bioscience 2024-08, Vol.60, p.104407, Article 104407
• Main Authors: Yang, Feiyan, Chu, Zhongxing, Wu, Qi, Qu, Guangfan, He, Zeyu, An, Jun, Tang, Yiping, Sun, Shuguo, Ci, Dun, Luo, Feijun
• Format: Article
• Language: English
• Subjects: Hypoxia; Mitochondria-dependent apoptosis; Molecular docking; Network pharmacology; Peptide; Renal injury
• ISSN: 2212-4292; 2212-4306
• DOI: 10.1016/j.fbio.2024.104407

Chronic kidney disease is a prevalent and severe significant complication of hypoxia. This study found that peptide LVYPFPGPIPN could protect hypoxia-induced renal injury in the animal model. Network pharmacology and molecular docking analysis indicated that cathepsin B (CTSB) and interleukin-1β (IL-1β) represent potential targets for the prevention/treatment of hypoxic-induced renal injury. GO analysis revealed the involvement of these genes in various biological processes, including apoptosis regulation, oxidative stress response, and adaptive immune modulation. Experimental results in vitro and in vivo demonstrated that peptide LVYPFPGPIPN could effectively inhibit apoptosis and stress responses of kidney cells by regulating the NRF2/IL-1β/mitochondrial apoptosis pathway, thereby protecting hypoxic human embryonic kidney cells from damage. The anti-hypoxic effect of the LVYPFPGPIPN offers a novel therapeutic clue for the treatment/prevention of hypoxic-induced kidney injury and inflammation-associated chronic kidney disease. [Display omitted]