ArticleEvidence-based complementary and alternative medicine : eCAM2016
Uliginosin B, a Possible New Analgesic Drug, Acts by Modulating the Adenosinergic System.
Article in Evidence-based complementary and alternative medicine : eCAM, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Evaluation of Uliginosin B as a Modulator of the Ras Pathway: In Vivo Evidence From Caenorhabditis elegans and In Silico Insights.Chemistry & biodiversity · 2026Article
- Valerenic Acid and Pinoresinol as Positive Allosteric Modulators: Unlocking the Sleep-Promoting Potential of Valerian Extract Ze 911.Molecules (Basel, Switzerland) · 2025Article
- Review
- Antinociceptive Activity of Petroleum Ether Fraction ofBioMed research international · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uliginosin B (ULI) is a natural acylphloroglucinol that has been proposed as a new molecular scaffold for developing analgesic and antidepressant drugs. Its effects seem to be due to its ability to increase monoamines in the synaptic cleft by inhibiting their neuronal uptake without binding to their respective transporters, but its exact mode of action is still unknown. Considering the importance of the purinergic system to pain transmission and its modulation by monoamines availability, the aim of this study was to investigate the involvement of adenosinergic signaling in antinociceptive effect of uliginosin B. The selective adenosine A1 receptor antagonist DPCPX and the selective A2A antagonist ZM 241385 prevented the effect of ULI in the hot-plate test in mice. Pretreatment with inhibitors of adenosine reuptake (dipyridamole) or adenosine deaminase (EHNA) did not affect the ULI effect. On the other hand, its effect was completely prevented by an inhibitor of ecto-5'-nucleotidase (AMPCP). This finding was confirmed ex vivo, whereby ULI treatment increased AMP and ATP hydrolysis in spinal cord and cerebral cortex synaptosomes, respectively. Altogether, these data indicate that activation of A1 and A2A receptors and the modulation of ecto-5'-nucleotidase activity contribute to the antinociceptive effect of ULI.
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Registered trials
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