LPS-Induced Liver Inflammation Is Inhibited by Psilocybin and Eugenol in Mice
Gregory Ian Robinson, Marta Gerasymchuk, Timur Zanikov, Esmaeel Ghasemi Gojani, Shima Asghari, Alyssa Groves, Lucie Haselhorst, Sanjana Nandakumar, Cora Stahl, Mackenzie Cameron, Yeva Zahoruiko, Dongping Li, Alex Snelling, Darryl Hudson, Anna Fiselier, Olga Kovalchuk, Igor Kovalchuk, Carlos Cruz, Rocio Rodriguez‐juarez
Pharmaceuticals March 23, 2025 DOI: 10.3390/ph18040451 via OpenAlex
Summary
AI-generated from the abstractPsilocybin and eugenol, both individually and combined, reduced inflammation in a mouse model of liver injury induced by lipopolysaccharides. Post-treatment administration produced stronger anti-inflammatory effects than pre-treatment. Psilocybin alone showed the most pronounced reduction of pro-inflammatory cytokines IL-1β, IL-6, and MCP-1, while the combination with eugenol (1:50 ratio) also strongly reduced COX-2 and TNF-α. Histological analysis indicated improved nuclear circularity and less inflammatory infiltration. Eugenol alone increased MCP-1 and GM-CSF, an adverse effect that was mitigated by co-administration with psilocybin. The findings suggest psilocybin and its combination with eugenol as potential therapies for hepatic inflammation.
Study at a glance
| Characteristics | Randomized controlled trial Peer reviewed |
|---|---|
| Population | C57BL/6J mice |
| Interventions | Psilocybin Eugenol |
| Dose | 0.88 mg/kg psilocybin, 17.59 mg/kg eugenol |
| Topics | Psilocybin |
| Keywords | Eugenol Inflammation Pharmacology Medicine |
| Citations | 4 |
| Key finding | Psilocybin and eugenol, alone or in combination, reduced LPS-induced liver inflammation in mice, with psilocybin alone showing the strongest anti-inflammatory effects. |
Abstract
Background/Objectives: Liver inflammatory diseases are a major global health burden and are often exacerbated by inflammation driven by lipopolysaccharides (LPS) through toll-like receptor 4 signaling. This study evaluates the anti-inflammatory effects of psilocybin and eugenol in an LPS-induced liver inflammation model in C57BL/6J mice. Methods: Mice were treated with psilocybin (0.88 mg/kg) and/or eugenol (17.59 mg/kg) either before (pre-treatment) or after (post-treatment) LPS injection. Results: Psilocybin and eugenol, individually and in combination, significantly reduced the LPS-induced mRNA levels of pro-inflammatory cytokines, with post-treatment administration exhibiting stronger effects than pre-treatment. Psilocybin alone displayed the most pronounced anti-inflammatory response, especially for IL-1β, IL-6, and MCP-1, while its combination with eugenol in 1:50 ratio demonstrated similar results, with strongly reduced COX-2 and TNF-α. Histological analysis revealed improved nuclear circularity and reduced inflammatory infiltration in the treatment groups. Eugenol alone showed potential adverse effects, including increased MCP-1 and GM-CSF, but this was mitigated by the co-administration of psilocybin. Conclusions: These findings highlight psilocybin and its combination with eugenol as promising therapies for hepatic inflammation, suggesting their application in treating acute and chronic liver diseases. Future research should explore their long-term effects, the mechanisms underlying their anti-inflammatory actions, and their therapeutic efficacy in humans.