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Peer-reviewedCC BY-NC 3.0Chemical Science

Bioorthogonal dual-channel imaging of NO and H2S reveals redox imbalance in atherosclerotic plaques

  • Jiheng Xu1,2
  • Xin Xia1
  • Ping Li1
  • Yue Tang3
  • Wen Zhang1
  • Hui Wang1
  • Wei Zhang1
  • Bo Tang1,2,4
4 affiliations
  1. 1College of Chemistry, Chemical Engineering and Materials Science, Collaborative Innovation Center of Functionalized Probes for Chemical Imaging in Universities of Shandong, Key Laboratory of Molecular and Nano Probes, Ministry of Education, Institute of Biomedical Sciences, Shandong Normal University Jinan 250014 P. R. China
  2. 2School of Materials Science and Engineering, Shandong University Jinan 250061 P. R. China
  3. 3Department of Emergency Medicine, Shandong Provincial Clinical Research Center for Emergency and Critical Care Medicine, Qilu Hospital of Shandong University Jinan 250014 P. R. China
  4. 4Laoshan Laboratory Qingdao 266237 P. R. China
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Abstract

Redox imbalance is closely associated with atherosclerosis (AS), but tools for precise, simultaneous, and in situ imaging of oxidative NO and reductive H2S within the AS plaque microenvironment are still lacking. Herein, we developed a bioorthogonal small-molecule fluorescent probe, DBCO-BOD-NH, for dual-channel imaging of NO and H2S. The probe is built on a BODIPY fluorophore, incorporates a dibenzocyclooctyne (DBCO) bioorthogonal group, and combines metabolic labeling with an unnatural sugar (N3-AC4GlcN). Through a “recognition-reporting” separation strategy, it achieves high signal-to-noise, synchronous imaging of both gasotransmitters in the plaque microenvironment. In vitro, the probe exhibits excellent optical properties, high selectivity, and good photostability. Cellular imaging reveals a dynamic inverse evolution during macrophage-to-foam cell transformation: NO levels gradually increase while H2S levels decrease. In animal models of AS and diabetes-combined AS, plaque progression is accompanied by increased NO and decreased H2S levels, and diabetes further exacerbates the NO-H2S redox homeostasis imbalance. This study not only provides a dual-channel imaging tool to investigate the dynamic evolution of NO-H2S imbalance in the AS plaque microenvironment, but also offers reliable evidence for the direct involvement of gasotransmitters in diabetes-accelerated AS progression.

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Cite

BibTeXRIS
BibTeX
@article{xu2026bioorthogonal,
  title = {{Bioorthogonal dual-channel imaging of NO and H2S reveals redox imbalance in atherosclerotic plaques}},
  author = {Jiheng Xu and Xin Xia and Ping Li and Yue Tang and Wen Zhang and Hui Wang and Wei Zhang and Bo Tang},
  journal = {Chemical Science},
  year = {2026},
  month = sep,
  doi = {10.1039/d6sc06239c},
  url = {https://doi.org/10.1039/d6sc06239c},
  note = {CC BY-NC 3.0},
}
RIS
TY  - JOUR
TI  - Bioorthogonal dual-channel imaging of NO and H2S reveals redox imbalance in atherosclerotic plaques
AU  - Jiheng Xu
AU  - Xin Xia
AU  - Ping Li
AU  - Yue Tang
AU  - Wen Zhang
AU  - Hui Wang
AU  - Wei Zhang
AU  - Bo Tang
PY  - 2026
DA  - 2026/09/01
JO  - Chemical Science
DO  - 10.1039/d6sc06239c
UR  - https://doi.org/10.1039/d6sc06239c
AB  - Redox imbalance is closely associated with atherosclerosis (AS), but tools for precise, simultaneous, and in situ imaging of oxidative NO and reductive H2S within the AS plaque microenvironment are still lacking. Herein, we developed a bioorthogonal small-molecule fluorescent probe, DBCO-BOD-NH, for dual-channel imaging of NO and H2S. The probe is built on a BODIPY fluorophore, incorporates a dibenzocyclooctyne (DBCO) bioorthogonal group, and combines metabolic labeling with an unnatural sugar (N3-AC4GlcN). Through a “recognition-reporting” separation strategy, it achieves high signal-to-noise, synchronous imaging of both gasotransmitters in the plaque microenvironment. In vitro, the probe exhibits excellent optical properties, high selectivity, and good photostability. Cellular imaging reveals a dynamic inverse evolution during macrophage-to-foam cell transformation: NO levels gradually increase while H2S levels decrease. In animal models of AS and diabetes-combined AS, plaque progression is accompanied by increased NO and decreased H2S levels, and diabetes further exacerbates the NO-H2S redox homeostasis imbalance. This study not only provides a dual-channel imaging tool to investigate the dynamic evolution of NO-H2S imbalance in the AS plaque microenvironment, but also offers reliable evidence for the direct involvement of gasotransmitters in diabetes-accelerated AS progression.
SN  - 2041-6520
SN  - 2041-6539
ER  -