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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