KNC nanozyme repairs hypoxia ischemia brain damage through ALOX12 mediated lipid peroxidation inhibition

Hypoxia-Ischemia Brain Damage (HIBD) results in a widespread neuronal damage and permanent brain tissue injury due to the severe reactive oxygen species (ROS) boost induced neuroinflammation. In this work, a K doped N-C based nanozyme was fabricated for scavenging ROS. KNC could impair ROS production and M1 polarization in microglia. Beneficial from these contents, the brain damage was mitigated in HIBD rats, which was proved by the increased regional blood flow, decreased pro-inflammatory microglia and astrocyte activation. The learning and memory capabilities were restored after applying with KNC post HIBD, which was ascribed to the diminished HI-induced dendritic spine loss in hippocampal regions. RNA-seq revealed that decreased ALOX12 expression is one of the clues of neuronal protection. KNC could combine with ALOX12 and further inhibit the lipid peroxidation. These two clues obtain KNC with superior ability of inhibition of ROS boost induced brain damage post HIBD. This nanozyme provided a potential strategies and new idea of HIBD therapy.

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Publication Details

Journal
Bioactive Materials
Published
2025-09-02
DOI
https://doi.org/10.1016/j.bioactmat.2025.08.032
Primary Topic
Advanced Nanomaterials in Catalysis
Type
article
Field-Weighted Citation Impact
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article

KNC nanozyme repairs hypoxia ischemia brain damage through ALOX12 mediated lipid peroxidation inhibition

Kwk Yeung, Liping Ouyang, Dongya Jiang, Yun Liao et al.
Bioactive Materials
Advanced Nanomaterials in Catalysis
article

KNC nanozyme repairs hypoxia ischemia brain damage through ALOX12 mediated lipid peroxidation inhibition

Kwk Yeung, Liping Ouyang, Dongya Jiang, Yun Liao, Xuanyong Liu, Ji Tan, Xiaohua Dong, Shuhan Chen, Xingdan Liu, Jing Zhao, Ziyi Lu
article en

Abstract

Hypoxia-Ischemia Brain Damage (HIBD) results in a widespread neuronal damage and permanent brain tissue injury due to the severe reactive oxygen species (ROS) boost induced neuroinflammation. In this work, a K doped N-C based nanozyme was fabricated for scavenging ROS. KNC could impair ROS production and M1 polarization in microglia. Beneficial from these contents, the brain damage was mitigated in HIBD rats, which was proved by the increased regional blood flow, decreased pro-inflammatory microglia and astrocyte activation. The learning and memory capabilities were restored after applying with KNC post HIBD, which was ascribed to the diminished HI-induced dendritic spine loss in hippocampal regions. RNA-seq revealed that decreased ALOX12 expression is one of the clues of neuronal protection. KNC could combine with ALOX12 and further inhibit the lipid peroxidation. These two clues obtain KNC with superior ability of inhibition of ROS boost induced brain damage post HIBD. This nanozyme provided a potential strategies and new idea of HIBD therapy.

Bioactive MaterialsVol. 54
Donghua University (CN), Shanghai Jiao Tong University (CN), Nanjing Children's Hospital (CN), Nanjing Maternity and Child Health Care Hospital (CN), Tongren Hospital (CN), University of Hong Kong - Shenzhen Hospital (CN), Shanghai Institute of Ceramics (CN), University of Hong Kong (HK)
Openalex Percentile: Top 83%
Advanced Nanomaterials in Catalysis
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