# Promoting spinal cord injury repair by using ZnO@MOFs nanozymes functionalized hydrogel through the ROS microenvironment regulating pathway

**Authors:** Jiaxin Ding, Binbin Gao, Zelin Sang, Zhen Dai, Zhenhua Chen, Xifan Mei

PMC · DOI: 10.1093/rb/rbaf095 · 2025-09-13

## TL;DR

This study introduces a new hydrogel-based nanotherapeutic system that reduces oxidative stress and neuronal death in spinal cord injuries using near-infrared light.

## Contribution

A novel ZnO-ZIF8@H nanotherapeutic system is developed to regulate the oxidative stress microenvironment in spinal cord injury repair.

## Key findings

- ZnO-ZIF8@H with NIR irradiation significantly reduced oxidative stress markers like MDA in injured tissues.
- The treatment enhanced antioxidant enzyme activity, including SOD and GSH, and suppressed neuronal apoptosis.
- TUNEL staining and Cleaved-Caspase3 analysis confirmed reduced neuronal death following the treatment.

## Abstract

Spinal cord injury (SCI) is a kind of health problem characterized by oxidative stress and neuronal apoptosis, which pose major challenges to the recovery of patients. Recently, the application of photothermal nanotechnology in medicine has opened up exciting new avenues for the treatment of SCI. This innovative approach leverages the unique properties of nanomaterials to enhance therapeutic outcomes. In our study, we developed a novel nanotherapeutic system named ZnO-ZIF8@H, which is designed to deliver targeted neuroprotective effects. We meticulously evaluated its performance under near-infrared (NIR) irradiation, which is known to promote local heating and stimulate biological processes. The data indicated that the application of ZnO-ZIF8@H combined with NIR irradiation significantly reduced oxidative stress levels in the affected tissues. This was evidenced by a marked decrease in malondialdehyde (MDA) levels, a well-known indicator of lipid peroxidation and cellular damage. Simultaneously, the treatment notably enhanced the activity of superoxide dismutase (SOD) and glutathione (GSH) enzymes. These findings suggest that ZnO-ZIF8@H+NIR could both protect cells from oxidative damage and boost the internal antioxidant defenses, highlighting its potential as an effective therapeutic strategy for mitigating secondary injuries following spinal cord trauma. It also suppressed neuronal apoptosis, as evidenced by TUNEL staining and decreased Cleaved-Caspase3 expression in NeuN-positive neurons. These results indicated that ZnO-ZIF8@H+NIR effectively reduces secondary damage from SCI by alleviating apoptosis and oxidative stress, offering a promising approach for the therapy of SCI.

## Linked entities

- **Proteins:** SOD1 (superoxide dismutase 1), LOC23687505 (pyrimidodiazepine synthase)
- **Chemicals:** malondialdehyde (PubChem CID 10964), glutathione (PubChem CID 124886)
- **Diseases:** spinal cord injury (MONDO:0043797)

## Full-text entities

- **Genes:** SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}, RBFOX3 (RNA binding fox-1 homolog 3) [NCBI Gene 146713] {aka FOX-3, FOX3, HRNBP3, NEUN}, CASP3 (caspase 3) [NCBI Gene 836] {aka CPP32, CPP32B, SCA-1}
- **Diseases:** SCI (MESH:D013119)
- **Chemicals:** MDA (MESH:D008315), ROS (-), GSH (MESH:D005978), ZnO (MESH:D015034), lipid (MESH:D008055)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

10 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12582391/full.md

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Source: https://tomesphere.com/paper/PMC12582391