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作 者:Feiyan Zhu Jiuyang He Lingfei Kong Zhanjun Guo Pengpeng Liang Jianlin Zhang Xiangming Wang Minmin Liang
机构地区:[1]Experimental Center of Advanced Materials,School of Materials Science&Engineering,Beijing Institute of Technology,Beijing 100081,China [2]National Laboratory of Biomacromolecules,Institute of Biophysics,Chinese Academy of Sciences,Beijing 100101,China [3]Center of Basic Medical Research,Institute of Medical Innovation and Research,Peking University Third Hospital,Beijing 100191,China [4]College of Rehabilitation Engineering,China Civil Affairs University,Beijing 102600,China [5]Beijing Key Laboratory of Cancer Invasion and Metastasis Research,School of Basic Medical Sciences,Capital Medical University,Beijing 100069,China
出 处:《Nano Research》2025年第2期641-649,共9页纳米研究(英文版)
基 金:This work was supported by the National Key R&D Program of China(No.2022YFA1205801);National Natural Science Foundation of China(Nos.T2225026,82172087,82071308,and 82404099);Peking University Third Hospital Clinical Key Project(Nos.BYSYZD2023041 and BYSYRCYJ2023004);Beijing Institute of Technology Research Fund Program for Young Scholars,and Outstanding Young Talent Project of Capital Medical University.
摘 要:It is well reported that cellular ferritin reduces the intracellular oxidative stress by sequestering excess ferrous ions,preventing them from participating in Fenton reactions that generate damaging harmful reactive oxygen species(ROS).Here we show a novel property of the native human ferritin H subunit nanoparticles(HFn NPs),which can function as catalase by effectively decomposing H_(2)O_(2) into H_(2)O and O_(2) in vivo that plays an important role in maintaining cellular redox homeostasis and in disease resistance.It was revealed that the catalase-like activity of HFn can be greatly increased by loading iron ions within the cavity of HFn nanocage.Moreover,HFn and iron-loaded HFn(HFn-Fe)can largely eliminate the oxidative damage caused by excess H_(2)O_(2) to live cells or Caenorhabditis elegans(C.elegans).Feeding HFn or HFn-Fe to C.elegans A30P Parkinson’s disease(PD)model significantly ameliorated theα-synuclein toxicity and alleviated the dendrite dysfunction in C.elegans PD models by substantively scavenging the in vivo H_(2)O_(2).This work demonstrates that the revealed novel catalase-like property of native HFn and HFn-Fe NPs may play an important role in maintaining cellular redox homeostasis and can be used as an effective therapeutic strategy against neurodegenerative diseases caused by redox dysregulation.
关 键 词:ANTIOXIDANT H-ferritin nanozymes oxidative damage treatment of Parkinson's disease
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