Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy · 2025
Nafamostat Mesylate Protects Against Acute Renal Ischemia-Reperfusion Injury by Alleviating Mitochondrial Dysfunction, Inhibiting Ferroptosis, and Regulating Proximal Tubular Cells: A Multi-Omics Analysis.
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Wang Yu, Wu Yuxuan, Li Hongqian, Liu Jiang, Chen Bo, Li Ying, Wang Qiaoyu, Zhang Dongmei, Huang Lan, Xing Huameng, Ou Santao, Xue Ling, Wu Weihua
Аннотация
OBJECTIVE: The present study aims to explore the role of nafamostat mesylate (NM) in ischemia-reperfusion (I/R)-induced acute kidney injury (AKI).
METHODS: Twenty-one male rats were randomly divided into three groups: sham, I/R, and I/R + NM groups. Acute renal I/R injury models were created in the I/R and I/R + NM groups by right nephrectomy and clamping the left renal pedicle for 45 min. Rats in the I/R + NM group were intraperitoneally injected with 0.75 mg/kg of NM before modeling. Blood and kidney specimens were collected at 24 h after model establishment. RNA sequencing (RNA-seq), KEGG and GO enrichment analyses, and single-cell sequencing were carried out to investigate the related mechanisms.
RESULTS: The pretreatment with NM improved renal function, reduced mitochondrial damage, suppressed the accumulation of reactive oxygen species, and inhibited ferroptosis. The RNA-seq indicated that NM induced protection by upregulating fatty acids, inhibiting inflammation, and promoting DNA repair. Proximal tubular cells were mainly affected.
CONCLUSION: NM protects against AKI by reducing reactive oxygen species, upregulating fatty acids, and regulating ferroptosis signaling pathways in proximal tubular cells.
METHODS: Twenty-one male rats were randomly divided into three groups: sham, I/R, and I/R + NM groups. Acute renal I/R injury models were created in the I/R and I/R + NM groups by right nephrectomy and clamping the left renal pedicle for 45 min. Rats in the I/R + NM group were intraperitoneally injected with 0.75 mg/kg of NM before modeling. Blood and kidney specimens were collected at 24 h after model establishment. RNA sequencing (RNA-seq), KEGG and GO enrichment analyses, and single-cell sequencing were carried out to investigate the related mechanisms.
RESULTS: The pretreatment with NM improved renal function, reduced mitochondrial damage, suppressed the accumulation of reactive oxygen species, and inhibited ferroptosis. The RNA-seq indicated that NM induced protection by upregulating fatty acids, inhibiting inflammation, and promoting DNA repair. Proximal tubular cells were mainly affected.
CONCLUSION: NM protects against AKI by reducing reactive oxygen species, upregulating fatty acids, and regulating ferroptosis signaling pathways in proximal tubular cells.