Xia Fan, Xiang Shanshan, Qiu Yihe, Lou Haiya, Wang Shuaifei, Liu Yupeng, Yu Fangying, Li Shiyan
Department of Ultrasound in Medicine, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, China.
Department of Pharmacy, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, China.
Adv Healthc Mater. 2025 Apr;14(10):e2405090. doi: 10.1002/adhm.202405090. Epub 2025 Feb 5.
Oxidative stress plays a critical role in the pathogenesis of ischemia-reperfusion injury (IRI)-induced acute kidney injury (AKI), driving necrosis of proximal tubule cells, inflammation, and capillary rarefaction. Inadequate perfusion resulting from capillary rarefaction can, in turn, induce chronic tissue hypoxia and exacerbate ischemic acute tubular necrosis, leading to an "oxidative stress-microvascular perfusion" negative feedback that further aggravate kidney damage. In this study, a macrophage membrane-camouflaged manganese-based antioxidant nanozyme (MB@LM) is developed for targeted delivery and oxidative stress relief in AKI therapy. By inheriting macrophage surface proteins, MB@LM selectively targets damaged renal tissues that overexpress adhesion molecules like intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), facilitating enhanced accumulation at the injury site. The manganese-based nanozyme core provides antioxidant enzyme-mimicking activities, effectively reducing oxidative stress and inhibiting apoptosis. In IRI-induced AKI mouse model, MB@LM treatment significantly reduces renal damage, restores renal microvascular perfusion as assessed by ultrasound imaging, and alleviated inflammation, demonstrating remarkable therapeutic efficacy. Overall, MB@LM represents a promising targeted therapy for AKI, offering precise delivery, potent antioxidant protection, and anti-inflammatory effects to support renal recovery and improve outcomes for AKI.
氧化应激在缺血再灌注损伤(IRI)诱导的急性肾损伤(AKI)发病机制中起关键作用,导致近端肾小管细胞坏死、炎症和毛细血管稀疏。毛细血管稀疏导致的灌注不足反过来又会诱发慢性组织缺氧并加重缺血性急性肾小管坏死,从而形成“氧化应激-微血管灌注”负反馈,进一步加重肾脏损伤。在本研究中,开发了一种巨噬细胞膜伪装的锰基抗氧化纳米酶(MB@LM),用于在AKI治疗中进行靶向递送和缓解氧化应激。通过继承巨噬细胞表面蛋白,MB@LM选择性地靶向过度表达细胞间粘附分子-1(ICAM-1)和血管细胞粘附分子-1(VCAM-1)等粘附分子的受损肾组织,促进在损伤部位的积累增加。锰基纳米酶核心具有模拟抗氧化酶的活性,有效降低氧化应激并抑制细胞凋亡。在IRI诱导的AKI小鼠模型中,MB@LM治疗显著减轻肾脏损伤,通过超声成像评估恢复肾微血管灌注,并减轻炎症,显示出显著的治疗效果。总体而言,MB@LM是一种有前景的AKI靶向治疗方法,提供精确递送、强大的抗氧化保护和抗炎作用,以支持肾脏恢复并改善AKI的治疗结果。