Melanin-like nanoparticles alleviate ischemiareperfusion injury in the kidney by scavenging reactive species and ferroptosis

被引:3
|
作者
Feng, Wenxiang [1 ]
Zhu, Nan [2 ]
Xia, Yubin [3 ]
Huang, Zehai [2 ]
Hu, Jianmin [1 ]
Guo, Zefeng [1 ]
Li, Yuzhuz [1 ]
Zhou, Song [1 ]
Liu, Yongguang [1 ]
Liu, Ding [1 ]
机构
[1] Southern Med Univ, Zhujiang Hosp, Sch Clin Med 2, Dept Organ Transplantat, Guangzhou 510515, Guangdong, Peoples R China
[2] Southern Med Univ, Nanfang Hosp, Sch Clin Med 1, Guangzhou 510515, Guangdong, Peoples R China
[3] Shantou Univ, Affiliated Hosp 1, Med Coll, Dept Nephrol, 57 Changping Rd, Shantou 515000, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Biological sciences; Biomedical materials; Drug delivery system; Nanoparticles;
D O I
10.1016/j.isci.2024.109504
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Kidney transplantation is essential for patients with end -stage renal disease; however, ischemia-reperfusion injury (IRI) during transplantation can lead to acute kidney damage and compromise survival. Recent studies have reported that antiferroptotic agents may be a potential therapeutic strategy, by reducing production of reactive oxygen species (ROS). Therefore, we constructed rutin -loaded polydopamine nanoparticles (PEG-PDA@rutin NPs, referred to as PPR NPs) to eliminate ROS resulting from IRI. Physicochemical characterization showed that the PPR NPs were - 100 nm spherical particles with good ROS scavenging ability. Notably, PPR NPs could effectively enter lipopolysaccharide (LPS)treated renal tubular cells, then polydopamine (PDA) released rutin to eliminate ROS, repair mitochondria, and suppress ferroptosis. Furthermore, in vivo imaging revealed that PPR NPs efficiently accumulated in the kidneys after IRI and effectively protected against IRI damage. In conclusion, PPR NPs demonstrated an excellent ability to eliminate ROS, suppress ferroptosis, and protect kidneys from IRI.
引用
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页数:15
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