Current Issues in Molecular Biology
August 15, 2023
Gregory Ian Robinson, Dongping Li, Bo Wang et al.
20 citations
Psilocybin (Psi) and eugenol (Eug) together reduced inflammation in human small intestinal epithelial cells. Cells were treated with inflammatory cytokines TNF-α and IFN-γ, then exposed to compounds targeting serotonin 2A receptors (Psi, 4-AcO-DMT, ketanserin) or transient receptor potential channels (capsaicin, curcumin, eugenol). Alone, Psi (40 μM), curcumin (0.5 μM), and eug (50 μM) lowered COX-2 protein without killing cells. The Psi–curcumin combination synergistically cut COX-2 by 28-fold but reduced IL-6 only 1.6-fold. The Psi–eug combination produced the best results: COX-2 dropped 19-fold and IL-6 dropped 10-fold, with no toxicity at any dose. This is the first work to examine psilocybin and 4-AcO-DMT's anti-inflammatory effects in intestinal cells.
Life
December 15, 2023
Gregory Ian Robinson, Dongping Li, Bo Wang et al.
19 citations
Psilocybin, 4-AcO-DMT, and eugenol significantly reduce levels of the inflammatory markers TNF-α and IFN-γ in human 3D EpiIntestinal tissue, while capsaicin and curcumin decrease these markers to a lesser extent. Psilocybin effectively lowers IL-6, IL-8, MCP-1, and GM-CSF levels, but curcumin, capsaicin, and 4-AcO-DMT have limited effects on these markers. Ketanserin lowers IL-6 and GM-CSF levels but has no effect on TNF-α, IFN-γ, IL-8, or MCP-1. Synergistic effects between 5-HT2A ligands and TRP channel ligands are minimal. The results provide further evidence of the anti-inflammatory effects of psilocybin and eugenol, though more research is needed on mechanisms and therapeutic feasibility for conditions like inflammatory bowel disease.
Psychoactives
January 28, 2024
Esmaeel Ghasemi Gojani, Bo Wang, Dongping Li et al.
12 citations
Psilocybin, a compound from Psilocybe mushrooms known for activating serotonin 5-HT2A receptors, reduces inflammation in immune cells. In laboratory experiments, human THP-1 monocytes were turned into macrophages and then stimulated with lipopolysaccharide (LPS) to trigger an inflammatory response, followed by adenosine triphosphate (ATP) to activate the NLRP3 inflammasome. Psilocybin exposure produced a dose-dependent inverse correlation with the production of proinflammatory cytokines and proteins. The compound likely mediates these anti-inflammatory effects by influencing key signaling pathways, including NF-κB, IL-6/TYK2/STAT3, and TYK2/STAT1.
Genes
January 29, 2024
Esmaeel Ghasemi Gojani, Bo Wang, Olga Kovalchuk et al.
11 citations
Psilocybin, a compound from Psilocybe mushrooms that activates serotonin receptors, may protect insulin-producing β-cells from damage caused by high glucose and high lipid conditions. In experiments with rat insulinoma cells, psilocybin pretreatment reduced cell loss, likely by altering apoptotic biomarkers and reducing phosphorylation of TXNIP, STAT-1, and STAT-3. It also modulated expression of genes linked to β-cell dedifferentiation, such as Pou5f1 and Nanog, suggesting it could help maintain β-cell identity. These findings indicate potential for psilocybin in treating Type II diabetes, though further research is needed.
Biochemistry and Cell Biology
January 1, 2025
Farzaneh Norouzkhani, Esmaeel Ghasemi Gojani, Bo Wang et al.
1 citation
A high-glucose and high-lipid diet accelerates cellular aging through oxidative stress, mitochondrial dysfunction, and inflammation, contributing to collagen degradation and skin aging. Psilocybin, a naturally occurring compound, was tested on BJ-5ta fibroblasts exposed to such conditions. Post-treatment with 15 µmol/L psilocybin and co-treatment with 10 µmol/L preserved cell viability and reduced senescence markers. The 10 µmol/L co-treatment most effectively lowered apoptosis and alleviated cell cycle arrest in S phase. Psilocybin also decreased inflammatory cytokines IL-1β, IL-6, and COX-2, and co-treatment significantly upregulated elastin gene expression, though fibroblast migration increased nonsignificantly. Psilocybin shows promise as a natural compound for reducing skin aging under oxidative stress.