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Peer-reviewedCC BY 4.0Molecules

Carbon Dots Derived from Carbonized Citri Reticulatae Pericarpium (Chenpi) Alleviate Metabolic Dysfunction-Associated Steatohepatitis

  • Juan Luo1
  • Xiangling Chen1
  • Ping Zhang2
  • Yuanchao Shi3
  • Yanling Li3
  • Peng Cui1,4
  • Qiongye Dong1
4 affiliations
  1. 1Precision Medicine Institute, Peking University Shenzhen Hospital, Shenzhen 518036, China
  2. 2Department of Hematology, Peking University Shenzhen Hospital, Shenzhen 518036, China
  3. 3Central Laboratory, Peking University Shenzhen Hospital, Shenzhen 518036, China
  4. 4Intervention and Cell Therapy Center, Peking University Shenzhen Hospital, Shenzhen 518036, China
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Abstract

Metabolic dysfunction-associated steatohepatitis (MASH) prevalence is rising globally, with approved targeted therapies associated with substantial adverse reactions. In this study, we synthesized carbon dots (CDs) derived from Citri Reticulatae Pericarpium (CRP-CDs) to investigate their safety and therapeutic effect against MASH. Here, novel CRP-CDs were synthesized via high-temperature carbonization and systematically characterized in terms of particle size, surface functional groups, and optical properties. We assessed the in vitro and in vivo biosafety of CRP-CDs. An FFA-induced fatty-degeneration HepG2 cell model was used to examine its regulation of hepatic lipid accumulation, while the HFD-induced mouse model was employed to evaluate its therapeutic efficacy against MASH. Data-independent acquisition mass spectrometry (DIA-MS) quantitative proteomics was performed to decipher its anti-MASH molecular mechanisms. The results showed that CRP-CDs displayed uniform particle size, abundant surface functional groups, and stable optical behaviors based on characterization tests. In vitro studies demonstrated that CRP-CDs exhibited excellent biocompatibility. CRP-CDs treatment effectively reduced intracellular TG and TC levels. Administration of CRP-CDs alleviated elevated serum biochemical parameters in HFD-induced MASH mice. Histological examination further revealed the protective effect of CRP-CDs on liver damage induced by HFD feeding. In addition, CRP-CDs decreased hepatic levels of IL-1β, IL-6, TNF-α, and MDA, and enhanced SOD activity as well as GSH content. Analysis of proteomic results demonstrated that CRP-CDs alleviated MASH pathogenesis via synergistic modulation of multiple signaling cascades rather than acting on a single pathway. Moreover, in vivo toxicity assessment validated the favorable systemic biosafety of CRP-CDs with no obvious adverse toxic effects in mice. In conclusion, novel CRP-CDs represent an environmentally friendly and biocompatible nanomaterial capable of effectively alleviating HFD-triggered MASH, which shows promise as a candidate for preclinical therapeutic development against fatty liver disease. Notably, these results are derived from preclinical short-term animal studies, and further validation is required prior to clinical translation.

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Cite

BibTeXRIS
BibTeX
@article{luo2026carbon,
  title = {{Carbon Dots Derived from Carbonized Citri Reticulatae Pericarpium (Chenpi) Alleviate Metabolic Dysfunction-Associated Steatohepatitis}},
  author = {Juan Luo and Xiangling Chen and Ping Zhang and Yuanchao Shi and Yanling Li and Peng Cui and Qiongye Dong},
  journal = {Molecules},
  year = {2026},
  month = oct,
  doi = {10.3390/molecules31213888},
  url = {https://www.mdpi.com/1420-3049/31/21/3888},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Carbon Dots Derived from Carbonized Citri Reticulatae Pericarpium (Chenpi) Alleviate Metabolic Dysfunction-Associated Steatohepatitis
AU  - Juan Luo
AU  - Xiangling Chen
AU  - Ping Zhang
AU  - Yuanchao Shi
AU  - Yanling Li
AU  - Peng Cui
AU  - Qiongye Dong
PY  - 2026
DA  - 2026/10/28
JO  - Molecules
DO  - 10.3390/molecules31213888
UR  - https://www.mdpi.com/1420-3049/31/21/3888
AB  - Metabolic dysfunction-associated steatohepatitis (MASH) prevalence is rising globally, with approved targeted therapies associated with substantial adverse reactions. In this study, we synthesized carbon dots (CDs) derived from Citri Reticulatae Pericarpium (CRP-CDs) to investigate their safety and therapeutic effect against MASH. Here, novel CRP-CDs were synthesized via high-temperature carbonization and systematically characterized in terms of particle size, surface functional groups, and optical properties. We assessed the in vitro and in vivo biosafety of CRP-CDs. An FFA-induced fatty-degeneration HepG2 cell model was used to examine its regulation of hepatic lipid accumulation, while the HFD-induced mouse model was employed to evaluate its therapeutic efficacy against MASH. Data-independent acquisition mass spectrometry (DIA-MS) quantitative proteomics was performed to decipher its anti-MASH molecular mechanisms. The results showed that CRP-CDs displayed uniform particle size, abundant surface functional groups, and stable optical behaviors based on characterization tests. In vitro studies demonstrated that CRP-CDs exhibited excellent biocompatibility. CRP-CDs treatment effectively reduced intracellular TG and TC levels. Administration of CRP-CDs alleviated elevated serum biochemical parameters in HFD-induced MASH mice. Histological examination further revealed the protective effect of CRP-CDs on liver damage induced by HFD feeding. In addition, CRP-CDs decreased hepatic levels of IL-1β, IL-6, TNF-α, and MDA, and enhanced SOD activity as well as GSH content. Analysis of proteomic results demonstrated that CRP-CDs alleviated MASH pathogenesis via synergistic modulation of multiple signaling cascades rather than acting on a single pathway. Moreover, in vivo toxicity assessment validated the favorable systemic biosafety of CRP-CDs with no obvious adverse toxic effects in mice. In conclusion, novel CRP-CDs represent an environmentally friendly and biocompatible nanomaterial capable of effectively alleviating HFD-triggered MASH, which shows promise as a candidate for preclinical therapeutic development against fatty liver disease. Notably, these results are derived from preclinical short-term animal studies, and further validation is required prior to clinical translation.
SN  - 1420-3049
ER  -