Regulation of inflammatory pathways by cannabigerol in the collagen induced arthritis model in rats
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60461373%3A22340%2F25%3A43933210" target="_blank" >RIV/60461373:22340/25:43933210 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216208:11110/25:10505764 RIV/00064165:_____/25:10505764
Výsledek na webu
<a href="https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2025.1705962/full" target="_blank" >https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2025.1705962/full</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3389/fphar.2025.1705962" target="_blank" >10.3389/fphar.2025.1705962</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Regulation of inflammatory pathways by cannabigerol in the collagen induced arthritis model in rats
Popis výsledku v původním jazyce
Objectives This study aims to assess the anti-inflammatory properties of cannabigerol (CBG) in collagen-induced arthritis (CIA) model in rats, and to determine which inflammatory signaling pathways it affects.Study design Rats were randomized into four groups: placebo (PCB)-p.o. Treated with 1 mL of 0.9% saline once daily, CBG-p.o. Treated with 30 mg of CBG/day, glucocorticoids (GC)-p.o. Treated with methylprednisolone 0.5 mg/kg/day, and negative control (CO)-p.o. Treated with 1 mL of 0.9% saline once daily. CIA was induced in the PCB, GC, and CBG groups. The effect of CBG was assessed by clinical scoring, paw width measurements, ELISA, and analysis of gene (qPCR) and protein (Western blot) expression of selected inflammatory markers in blood and synovial membrane.Results Clinical scores showed significant improvement in the CBG vs. PCB on day 29 and in the GC vs. PCB on days 24, 27, and 29. MMP-3 levels in serum were significantly reduced in the GC vs. PCB. CBG demonstrated a selective anti-inflammatory and immunomodulatory profile, notably through the downregulation of key signaling molecules such as TLRs, systemic NF-kappa B p65, STAT-3, and inflammasome-related components including NLRP1A, NLRP3, AIM2, gasdermin D, and caspase-1. It also reduced IL-1 beta and TNF expression during the early phase of disease and increased expression of the anti-apoptotic gene BCL-2.Conclusion Our findings indicate that CBG modulates distinct components of the inflammatory signaling pathways, and its effects translated into significant improvement in clinical scoring based on swelling, erythema, stiffness in rat CIA model.
Název v anglickém jazyce
Regulation of inflammatory pathways by cannabigerol in the collagen induced arthritis model in rats
Popis výsledku anglicky
Objectives This study aims to assess the anti-inflammatory properties of cannabigerol (CBG) in collagen-induced arthritis (CIA) model in rats, and to determine which inflammatory signaling pathways it affects.Study design Rats were randomized into four groups: placebo (PCB)-p.o. Treated with 1 mL of 0.9% saline once daily, CBG-p.o. Treated with 30 mg of CBG/day, glucocorticoids (GC)-p.o. Treated with methylprednisolone 0.5 mg/kg/day, and negative control (CO)-p.o. Treated with 1 mL of 0.9% saline once daily. CIA was induced in the PCB, GC, and CBG groups. The effect of CBG was assessed by clinical scoring, paw width measurements, ELISA, and analysis of gene (qPCR) and protein (Western blot) expression of selected inflammatory markers in blood and synovial membrane.Results Clinical scores showed significant improvement in the CBG vs. PCB on day 29 and in the GC vs. PCB on days 24, 27, and 29. MMP-3 levels in serum were significantly reduced in the GC vs. PCB. CBG demonstrated a selective anti-inflammatory and immunomodulatory profile, notably through the downregulation of key signaling molecules such as TLRs, systemic NF-kappa B p65, STAT-3, and inflammasome-related components including NLRP1A, NLRP3, AIM2, gasdermin D, and caspase-1. It also reduced IL-1 beta and TNF expression during the early phase of disease and increased expression of the anti-apoptotic gene BCL-2.Conclusion Our findings indicate that CBG modulates distinct components of the inflammatory signaling pathways, and its effects translated into significant improvement in clinical scoring based on swelling, erythema, stiffness in rat CIA model.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30100 - Basic medicine
Návaznosti výsledku
Projekt
<a href="/cs/project/NU22-08-00346" target="_blank" >NU22-08-00346: Kombinace nových derivátů kanabinoidů a pokročilých formulačních metod pro léčbu revmatoidní artritidy</a><br>
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
2025
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Frontiers in Pharmacology
ISSN
1663-9812
e-ISSN
1663-9812
Svazek periodika
16
Číslo periodika v rámci svazku
1705962
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
18
Strana od-do
nestránkováno
Kód UT WoS článku
001611244500001
EID výsledku v databázi Scopus
2-s2.0-105021524653