ArticleBMC complementary and alternative medicine2015
Fulvic acid attenuates homocysteine-induced cyclooxygenase-2 expression in human monocytes.
Article in BMC complementary and alternative medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 32 citations in OpenAlex.
- Integrated safety and microbiota profiling of fulvic acid formulations across in vitro and in vivo models.Scientific reports · 2026Article
- Biomedical Applications of Humic Substances: From Natural Biopolymers to Therapeutic Agents.Antioxidants (Basel, Switzerland) · 2025Review
- Natural fulvic acids inhibit non-small-cell lung cancer through the COX-2/PGE2/EP4 axis: In silico and in vivo assessments.Heliyon · 2023Article
- Fulvic Acid Attenuates Atopic Dermatitis by Downregulating CCL17/22.Molecules (Basel, Switzerland) · 2023Article
- Homocysteine Causes Endothelial Dysfunction via Inflammatory Factor-Mediated Activation of Epithelial Sodium Channel (ENaC).Frontiers in cell and developmental biology · 2021Article
- Health Beneficial Effects of Moomiaii in Traditional Medicine.Galen medical journal · 2020Review
- A Comprehensive Toxicological Assessment of Fulvic Acid.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Article
- Therapeutic Potential of Fulvic Acid in Chronic Inflammatory Diseases and Diabetes.Journal of diabetes research · 2018Review
- Penehyclidine Hydrochloride Preconditioning Provides Cardioprotection in a Rat Model of Myocardial Ischemia/Reperfusion Injury.PloS one · 2015Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHomocysteine and pro-inflammatory mediators such as cyclooxygenase-2 (COX-2) have been linked to vascular dysfunction and risks of cardiovascular diseases. Fulvic acid (FA), a class of compounds of humic substances, possesses various pharmacological properties. However, the effect of FA on inflammatory responses of the monocytes remains unclear. We investigated the regulatory effect of FA on homocysteine-induced COX-2 expression in human monocytes.
methodsPeripheral blood monocytes and U937 cells were used for all experiments. Real-time PCR and ELISA assay were used to analyze the COX-2 mRNA expression and PGE2 secretion, respectively. Specific inhibitors were used to investigate the mechanism of homocysteine-mediating COX-2 mRNA expression and PGE2 secretion. Luciferase assay, transcription factor ELISA, and chromatin immunoprecipitation were used to determine the role of nuclear factor-κB in FA-mediated inhibition of homocysteine effect on monocytes.
resultsThe results show that pretreating monocytes with FA inhibited the homocysteine-induced COX-2 expression in a dose-dependent manner. Stimulation of U937 monocytes with homocysteine induced rapid increases in the phosphorylation of ERK and JNK; the inhibitor for ERK and JNK attenuated the homocysteine-induced nuclear factor-κB activation and COX-2 expression. Transcription factor ELISA and chromatin immunoprecipitation assays showed that FA blocked the homocysteine-induced increases in the binding activity and in vivo promoter binding of nuclear factor-κB in monocytes.
conclusionsOur findings provide a molecular mechanism by which FA inhibits homocysteine-induced COX-2 expression in monocytes, and a basis for using FA in pharmaceutical therapy against inflammation.
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