Related Experiment Video
Updated: Apr 30, 2026
07:34
Use of Animal Model of Sepsis to Evaluate Novel Herbal Therapies
Published on: April 11, 2012
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Experimental cannabinoid 2 receptor-mediated immune modulation in sepsis
J Sardinha1, M E M Kelly1, J Zhou2
1Department of Pharmacology, Dalhousie University, Halifax, NS, Canada B3H 4R2.
Mediators of Inflammation
|May 8, 2014
Summary
Modulating the CB2 receptor pathway in sepsis shows promise. Activating CB2 receptors reduced inflammatory leukocyte interactions, but did not fully restore tissue damage in a mouse model, suggesting complex therapeutic potential.
Area of Science:
- Immunology
- Pharmacology
- Gastroenterology
Background:
- Sepsis involves a dysregulated immune response to infection, with high mortality.
- Current sepsis treatments are insufficient.
- The endocannabinoid system presents a potential therapeutic target for sepsis.
Purpose of the Study:
- To investigate the effects of modulating the CB2 receptor pathway on sepsis pathogenesis.
- To assess the impact of CB2 receptor agonists and antagonists on leukocyte-endothelial interactions and tissue damage in a mouse model of endotoxemia.
Main Methods:
- Acute sepsis was induced in mice via lipopolysaccharide (LPS) injection.
- Intestinal microcirculation was examined using intravital microscopy.
- The effects of CB2 receptor agonist (HU308), antagonist (AM630), FAAH inhibitor (URB597), and MAGL inhibitor (JZL184) were evaluated.
Main Results:
- HU308 reduced adherent leukocytes but did not restore villi FCD.
- AM630 maintained leukocyte adhesion and worsened villi FCD.
- URB597 and JZL184 reduced leukocyte adhesion but did not restore mucosal villi FCD.
Conclusions:
- Activating CB2 receptors can decrease leukocyte-endothelial interactions in sepsis.
- Targeting the CB2 receptor pathway offers potential for reducing inflammatory damage in sepsis.
- Further research is needed to fully restore tissue function during sepsis treatment.
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