A peptide from yak ameliorates hypoxia-induced kidney injury by inhibiting inflammation and apoptosis via Nrf2 pathway
文献类型: 外文期刊
作者: Yang, Feiyan 1 ; Chu, Zhongxing 1 ; Wu, Qi 1 ; Qu, Guangfan 1 ; He, Zeyu 1 ; An, Jun 1 ; Tang, Yiping 1 ; Sun, Shuguo 1 ; Ci, Dun 2 ; Luo, Feijun 1 ;
作者机构: 1.Cent South Univ Forestry & Technol, Hunan Key Lab Forestry Edible Resources Safety & P, Natl Engn Lab Deep Proc Rice & Byproducts, Hunan Key Lab Grain oil Deep Proc & Qual Control, Changsha 410004, Hunan, Peoples R China
2.Tibet Acad Agr & Anim Husb Sci, Inst Agr Qual Stand & Testing, Lhasa 850032, Xizang, Peoples R China
3.Cent South Univ Forestry & Technol, Coll Food Sci & Engn, 498 Shaoshan Rd, Changsha 410004, Hunan, Peoples R China
关键词: Peptide; Network pharmacology; Molecular docking; Hypoxia; Renal injury; Mitochondria -dependent apoptosis
期刊名称:FOOD BIOSCIENCE ( 影响因子:4.8; 五年影响因子:5.1 )
ISSN: 2212-4292
年卷期: 2024 年 60 卷
页码:
收录情况: SCI
摘要: 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-1 beta (IL-1 beta) 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-1 beta/mitochondrial apoptosis pathway, thereby protecting hypoxic human embryonic kidney cells from damage. The antihypoxic effect of the LVYPFPGPIPN offers a novel therapeutic clue for the treatment/prevention of hypoxicinduced kidney injury and inflammation-associated chronic kidney disease.
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