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Peer-reviewedCC BYJournal of Bioresources and Bioproducts

Bio-based protocatechuic acid-anchored multimetallic nanoreactors: Green construction, redox-cycling properties, and biomedical potential

  • Wanmei Zhou1
  • Litao Wang1
  • Chengdong Nie2
  • Zixin Wang3
  • Qi Gu1
  • Haiting Tian1
  • Chenlu Wang1
  • Thomas Efferth4
  • Yujie Fu
4 affiliations
  1. 1The College of Forestry, Beijing Forestry University, Beijing 100083, China; State Key Laboratory of Efficient Production of Forest Resources, Beijing Forestry University, Beijing 100083, China
  2. 2College of Chemistry, Chemical Engineering and Resource Utilization, Northeast Forestry University, Harbin 150040, China
  3. 3Institute of Integration of Traditional and Western Medicine, Guangzhou Medical University, Guangzhou 511436, China; Artemisinin Research Center, Guangzhou University of Chinese Medicine, Guangzhou 510006, China
  4. 4Department of Pharmaceutical Biology, Institute of Pharmaceutical and Biomedical Sciences, Johannes Gutenberg University, Mainz 55128, Germany
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Abstract

Tumor cells often develop reductive adaptations that decrease the effectiveness of reactive oxygen species (ROS)-dependent treatments, prompting a need for catalytic platforms that sustainably amplify redox stress. In this work, we constructed a bio-based protocatechuic acid (PCA)-anchored multimetallic Fe-based metal-organic framework (Fe-MOF) nanoreactor with magnetic resonance imaging (MRI) capability and redox-activated therapeutic potential. Combining the PCA-coordinated Fe 2+ /Fe 3+ framework with Cu + /Cu 2+ redox cycling and ultrasmall Au domains, this redox network formed a tightly interconnected Fe/Cu/Au catalytic system that supported Fenton-type conversion of H 2 O 2 into •OH, glutathione (GSH) depletion, and enhanced oxidative stress in tumor environments. The addition of the natural compound brazilin (BRA) promoted apoptosis and enhanced the sensitivity of tumor cells to ferroptosis. Surface coating with homotypic 4T1 cell membranes enabled tumor homing and facilitated BRA release within tumors. Mechanistically, the nanoreactor perturbed cellular redox regulation across multiple metabolic pathways, including reduced expression of cytochrome c oxidase subunit 4 isoform 1 (COX4I1), serine hydroxymethyltransferase 2 (SHMT2), and dihydroorotate dehydrogenase (DHODH), suppression of the glutathione peroxidase 4 (GPX4)-solute carrier family 7 member 11 (SLC7A11) antioxidant response, and acyl-CoA synthetase long-chain family member 4 (ACSL4)-mediated lipid remodeling. In general, PCA-ligated Fe-MOF sequentially modified with Au, Cu, BRA, and 4T1 cell membranes (FP@ACBM) enhanced ROS accumulation, promoted lipid peroxidation, and induced apoptosis, thus producing antitumor effects. At the same time, it enabled stable longitudinal relaxation time ( T 1 )-weighted MRI contrast enhancement. Overall, this bio-based phenolic ligand-assembled mixed-valence Fe-MOF platform provides a versatile strategy for constructing redox-cycling nanomaterials with promising biomedical applications.

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Cite

BibTeXRIS
BibTeX
@article{zhou2026biobased,
  title = {{Bio-based protocatechuic acid-anchored multimetallic nanoreactors: Green construction, redox-cycling properties, and biomedical potential}},
  author = {Wanmei Zhou and Litao Wang and Chengdong Nie and Zixin Wang and Qi Gu and Haiting Tian and Chenlu Wang and Thomas Efferth and Yujie Fu},
  journal = {Journal of Bioresources and Bioproducts},
  year = {2026},
  month = oct,
  doi = {10.1016/j.jobab.2026.100298},
  url = {https://doi.org/10.1016/j.jobab.2026.100298},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Bio-based protocatechuic acid-anchored multimetallic nanoreactors: Green construction, redox-cycling properties, and biomedical potential
AU  - Wanmei Zhou
AU  - Litao Wang
AU  - Chengdong Nie
AU  - Zixin Wang
AU  - Qi Gu
AU  - Haiting Tian
AU  - Chenlu Wang
AU  - Thomas Efferth
AU  - Yujie Fu
PY  - 2026
DA  - 2026/10/25
JO  - Journal of Bioresources and Bioproducts
DO  - 10.1016/j.jobab.2026.100298
UR  - https://doi.org/10.1016/j.jobab.2026.100298
AB  - Tumor cells often develop reductive adaptations that decrease the effectiveness of reactive oxygen species (ROS)-dependent treatments, prompting a need for catalytic platforms that sustainably amplify redox stress. In this work, we constructed a bio-based protocatechuic acid (PCA)-anchored multimetallic Fe-based metal-organic framework (Fe-MOF) nanoreactor with magnetic resonance imaging (MRI) capability and redox-activated therapeutic potential. Combining the PCA-coordinated Fe 2+ /Fe 3+ framework with Cu + /Cu 2+ redox cycling and ultrasmall Au domains, this redox network formed a tightly interconnected Fe/Cu/Au catalytic system that supported Fenton-type conversion of H 2 O 2 into •OH, glutathione (GSH) depletion, and enhanced oxidative stress in tumor environments. The addition of the natural compound brazilin (BRA) promoted apoptosis and enhanced the sensitivity of tumor cells to ferroptosis. Surface coating with homotypic 4T1 cell membranes enabled tumor homing and facilitated BRA release within tumors. Mechanistically, the nanoreactor perturbed cellular redox regulation across multiple metabolic pathways, including reduced expression of cytochrome c oxidase subunit 4 isoform 1 (COX4I1), serine hydroxymethyltransferase 2 (SHMT2), and dihydroorotate dehydrogenase (DHODH), suppression of the glutathione peroxidase 4 (GPX4)-solute carrier family 7 member 11 (SLC7A11) antioxidant response, and acyl-CoA synthetase long-chain family member 4 (ACSL4)-mediated lipid remodeling. In general, PCA-ligated Fe-MOF sequentially modified with Au, Cu, BRA, and 4T1 cell membranes (FP@ACBM) enhanced ROS accumulation, promoted lipid peroxidation, and induced apoptosis, thus producing antitumor effects. At the same time, it enabled stable longitudinal relaxation time ( T 1 )-weighted MRI contrast enhancement. Overall, this bio-based phenolic ligand-assembled mixed-valence Fe-MOF platform provides a versatile strategy for constructing redox-cycling nanomaterials with promising biomedical applications.
SN  - 2369-9698
ER  -