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Peer-reviewedCC BY 4.0Frontiers in Pharmacology

Green edible crataegi fructus-derived carbon dots ameliorate hyperlipidemia via the PPARα signaling pathway

  • Guojiao Shang1
  • Yafang Zhao1,2
  • Ertong Dai1
  • Ruiyan Liu1
  • Minlong Xia1
  • Zixuan Lu1
  • Siqi Wang1
  • Bilin Jin1
  • Herui Huang1
  • Yue Zhang3
  • Hui Kong1
  • Huihua Qu4
1 more authors
  • Yan Zhao1
4 affiliations
  1. 1School of Traditional Chinese Medicine, Beijing University of Chinese Medicine
  2. 2School of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine
  3. 3School of Life Sciences, Beijing University of Chinese Medicine
  4. 4Center of Scientific Experiment, Beijing University of Chinese Medicine
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Abstract

Background: Hyperlipidemia (HL) is a lipid metabolism disorder that contributes significantly to the global burden of metabolic diseases. Hence, novel pharmacological interventions are urgently needed. Our study explored the potential mechanisms by which Crataegi Fructus Carbonisata carbon dots (CFC-CDs) act against hyperlipidemia through in vivo and in vitro experiments.

Methods: We prepared CFC-CDs and comprehensively characterized them. Subsequently, we assessed the effects of CFC-CDs on serum lipid profiles in a high-fat diet-induced rat model and used transcriptomic analysis to explore the potential mechanisms underlying their lipid-lowering effects. Additionally, we developed an in vitro model of sodium oleate (OA)-induced lipid deposition in HepG2 cells and validated it using the PPARα inhibitor GW6471.

Results: The CFC-CDs had an ultrasmall size ranging from 1.34 to 4.67 nm and an interplanar spacing of approximately 0.210 nm. Their surfaces contained functional groups, including–OH, C=O, and C=N. These CDs exhibited excellent biocompatibility. Animal studies demonstrated that oral treatment with CFC-CDs markedly reduced high-fat diet (HFD)-induced hyperlipidemia. Liver transcriptome analysis indicated that CFC-CDs exerted lipid-lowering effects primarily by activating the PPARα signaling pathway, suggesting that CFC-CDs have significant metabolic reprogramming capabilities. CFC-CDs also exhibited excellent lipid-lowering effects in vitro , and the PPARα inhibitor GW6471 reversed the protective effects of CFC-CDs, thereby leading to lipid accumulation. CFC-CDs may be a potential therapeutic agent for HL.

Conclusion: The above evidence suggests that CFC-CDs synthesized by one-step calcination can significantly improve lipid metabolism disorders. Our study shows that CFC-CDs are a biomass-derived carbonaceous nanomaterial exhibiting effective lipid-lowering properties and broadening their potential clinical applications. This research provides crucial insights into the use of CFC-CDs in metabolic disease treatment and lays a solid experimental foundation for developing a new lipid-lowering candidate.

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Cite

BibTeXRIS
BibTeX
@article{shang2026green,
  title = {{Green edible crataegi fructus-derived carbon dots ameliorate hyperlipidemia via the PPARα signaling pathway}},
  author = {Guojiao Shang and Yafang Zhao and Ertong Dai and Ruiyan Liu and Minlong Xia and Zixuan Lu and Siqi Wang and Bilin Jin and Herui Huang and Yue Zhang and Hui Kong and Huihua Qu and Yan Zhao},
  journal = {Frontiers in Pharmacology},
  year = {2026},
  month = oct,
  doi = {10.3389/fphar.2026.1985522},
  url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1985522/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Green edible crataegi fructus-derived carbon dots ameliorate hyperlipidemia via the PPARα signaling pathway
AU  - Guojiao Shang
AU  - Yafang Zhao
AU  - Ertong Dai
AU  - Ruiyan Liu
AU  - Minlong Xia
AU  - Zixuan Lu
AU  - Siqi Wang
AU  - Bilin Jin
AU  - Herui Huang
AU  - Yue Zhang
AU  - Hui Kong
AU  - Huihua Qu
AU  - Yan Zhao
PY  - 2026
DA  - 2026/10/16
JO  - Frontiers in Pharmacology
DO  - 10.3389/fphar.2026.1985522
UR  - https://www.frontiersin.org/articles/10.3389/fphar.2026.1985522/full
AB  - Background: Hyperlipidemia (HL) is a lipid metabolism disorder that contributes significantly to the global burden of metabolic diseases. Hence, novel pharmacological interventions are urgently needed. Our study explored the potential mechanisms by which Crataegi Fructus Carbonisata carbon dots (CFC-CDs) act against hyperlipidemia through in vivo and in vitro experiments.  Methods: We prepared CFC-CDs and comprehensively characterized them. Subsequently, we assessed the effects of CFC-CDs on serum lipid profiles in a high-fat diet-induced rat model and used transcriptomic analysis to explore the potential mechanisms underlying their lipid-lowering effects. Additionally, we developed an in vitro model of sodium oleate (OA)-induced lipid deposition in HepG2 cells and validated it using the PPARα inhibitor GW6471.  Results: The CFC-CDs had an ultrasmall size ranging from 1.34 to 4.67 nm and an interplanar spacing of approximately 0.210 nm. Their surfaces contained functional groups, including–OH, C=O, and C=N. These CDs exhibited excellent biocompatibility. Animal studies demonstrated that oral treatment with CFC-CDs markedly reduced high-fat diet (HFD)-induced hyperlipidemia. Liver transcriptome analysis indicated that CFC-CDs exerted lipid-lowering effects primarily by activating the PPARα signaling pathway, suggesting that CFC-CDs have significant metabolic reprogramming capabilities. CFC-CDs also exhibited excellent lipid-lowering effects in vitro , and the PPARα inhibitor GW6471 reversed the protective effects of CFC-CDs, thereby leading to lipid accumulation. CFC-CDs may be a potential therapeutic agent for HL.  Conclusion: The above evidence suggests that CFC-CDs synthesized by one-step calcination can significantly improve lipid metabolism disorders. Our study shows that CFC-CDs are a biomass-derived carbonaceous nanomaterial exhibiting effective lipid-lowering properties and broadening their potential clinical applications. This research provides crucial insights into the use of CFC-CDs in metabolic disease treatment and lays a solid experimental foundation for developing a new lipid-lowering candidate.
SN  - 1663-9812
ER  -