Abstract：
BACKGROUND: Renal ischemia-reperfusion injury (IRI) is one of the causes of acute kidney injury. Annexin A5 (AnxA5), a calcium-dependent cell membrane-binding protein, shows protective effects in various organ IRI models. This study explored the therapeutic effect of exogenous AnxA5 monomer protein on renal IRI and its potential mechanism of action.
RESULTS: Different doses of AnxA5 were injected intravenously to treat bilateral renal IRI in SD rats. This model confirmed the protective effects of AnxA5 on kidney structure and function. In vitro, HK-2 cells were subjected to hypoxia for 12 h, followed by restoration of normal oxygen supply to simulate IRI. In vitro experiments demonstrated the mechanism of action of AnxA5 by measuring cellular activity and permeability. A comparison of the mutant AnxA5 protein M23 and the application of a calcium-free culture medium further validated the protective effect of AnxA5 by forming a network structure.
CONCLUSIONS: Exogenous AnxA5 monomers prevented renal IRI by binding to the damaged renal tubular epithelial cell membrane, forming a two-dimensional network structure to maintain cell membrane integrity, and ultimately prevent cell death.
RESULTS: Different doses of AnxA5 were injected intravenously to treat bilateral renal IRI in SD rats. This model confirmed the protective effects of AnxA5 on kidney structure and function. In vitro, HK-2 cells were subjected to hypoxia for 12 h, followed by restoration of normal oxygen supply to simulate IRI. In vitro experiments demonstrated the mechanism of action of AnxA5 by measuring cellular activity and permeability. A comparison of the mutant AnxA5 protein M23 and the application of a calcium-free culture medium further validated the protective effect of AnxA5 by forming a network structure.
CONCLUSIONS: Exogenous AnxA5 monomers prevented renal IRI by binding to the damaged renal tubular epithelial cell membrane, forming a two-dimensional network structure to maintain cell membrane integrity, and ultimately prevent cell death.
摘要：
背景：肾缺血再灌注损伤（IRI）是急性肾损伤的原因之一。膜联蛋白A5(AnxA5),钙依赖性细胞膜结合蛋白，在各种器官IRI模型中显示保护作用。本研究探讨外源性AnxA5单体蛋白对肾脏IRI的治疗作用及其潜在作用机制。
结果：静脉注射不同剂量的AnxA5治疗SD大鼠双侧肾IRI。该模型证实了AnxA5对肾脏结构和功能的保护作用。体外，HK-2细胞缺氧12小时，然后恢复正常氧气供应以模拟IRI。体外实验通过测量细胞活性和通透性证明了AnxA5的作用机制。突变AnxA5蛋白M23的比较和无钙培养基的应用通过形成网络结构进一步验证了AnxA5的保护作用。
结论：外源性AnxA5单体通过与受损的肾小管上皮细胞膜结合来预防肾IRI，形成一个二维网络结构，以保持细胞膜的完整性，并最终防止细胞死亡。
结果：静脉注射不同剂量的AnxA5治疗SD大鼠双侧肾IRI。该模型证实了AnxA5对肾脏结构和功能的保护作用。体外，HK-2细胞缺氧12小时，然后恢复正常氧气供应以模拟IRI。体外实验通过测量细胞活性和通透性证明了AnxA5的作用机制。突变AnxA5蛋白M23的比较和无钙培养基的应用通过形成网络结构进一步验证了AnxA5的保护作用。
结论：外源性AnxA5单体通过与受损的肾小管上皮细胞膜结合来预防肾IRI，形成一个二维网络结构，以保持细胞膜的完整性，并最终防止细胞死亡。
