ArticleFrontiers in pharmacology2026
Safe dosage and potential risks of chlorogenic acid: insights from
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Recent Advances in Chlorogenic Acids for Food Preservation and Shelf-Life Extension.Antioxidants (Basel, Switzerland) · 2026Review
- Evaluation of Phytochemical Constituents, Antioxidant Potential, and Toxicological Profile of Selected Medicinal Plants from Romania's Spontaneous Flora.Molecules (Basel, Switzerland) · 2026Article
- Bioavailability of dietary polyphenols and plant bioactives in functional foods: insights and limitations fromFrontiers in nutrition · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: As the economy grows, there is a growing emphasis on food safety. While the health benefits of chlorogenic acid (CGA) are recognized, safe dosages and potential liver cell damage from excessive CGA consumption are not well studied. This study aims to determine the safe and effective dose range of CGA and understand how it causes toxicity in hepatocyte at half-maximal inhibitory concentration (IC50). Methods: This study assessed the impact of various CGA concentrations on liver cells, examining growth, viability, toxicity, energy metabolism, and colony formation using Real-Time Cell Analysis (RTCA), CCK-8, lactate dehydrogenase (LDH) assays, and Seahorse XF96. It established CGA's IC50 for cell viability and identified differentially expressed proteins via proteomics. Subsequently, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted to elucidate the signaling pathways associated with the differentially expressed proteins. Further validation of the molecular mechanisms was performed using flow cytometry, Western blotting, and reverse transcription quantitative polymerase chain reaction (RT-qPCR). Finally, CGA was injected into Kunming (KM) mice via the tail vein for acute toxicity testing. Results: In this study, 200 µM of CGA significantly reduced LDH release and increased the mitochondrial oxygen consumption rate (OCR) in hepatocytes, but it did not affect the extracellular acidification rate (ECAR). Additionally, 200 µM of CGA slightly promoted hepatocyte growth; however, at 300 μM, CGA nearly completely inhibited the clonogenic capacity of hepatocytes, and at 600 μM, it significantly impeded hepatocyte growth. The IC50 of CGA for hepatocyte activity was determined to be 613.1 µM. Conclusion: These findings suggest that the antioxidant and iron-chelating properties of CGA determine its role in either liver protection or toxicity at varying concentrations, providing valuable insight for its rational dietary and clinical use.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.