Study: Long-Term CB2R Activation “Might Prevent Neuroinflammation and Oxidative Stress-Associated Sickness Behavior”

marijuana card

Study: Long-Term CB2R Activation “Might Prevent Neuroinflammation and Oxidative Stress-Associated Sickness Behavior”

Activation of the cannabinoid receptor 2 (CB2R), something done naturally through the consumption of cannabis and cannabinoids, “might prevent neuroinflammation and oxidative stress-associated sickness behavior”, according to a new study.

The study, titled Cannabinoid receptor 2 activation mitigates lipopolysaccharide-induced neuroinflammation and sickness behavior in mice, is being published in the journal Psychopharmacology. It was epublished ahead of print by the U.S. National Institute of Health.

“Cannabinoid receptor 2 (CB2R) signaling in the brain is associated with the pathophysiology of depression”, states the study’s abstract. “Sickness behavior, characterized by lessened mobility, social interaction, and depressive behavior, is linked with neuroinflammation, oxidative stress, and immune system. The present study was aimed at evaluating 1-phenylisatin (PI), a CB2R agonist, in sickness behavior.”

For the study, “influence of acute and 7-day activation of CB2R using PI in lipopolysaccharide (LPS)-induced sickness behavior was assessed in mice.” An acute injection of LPS (1.5 mg/kg) “produced a fully developed sickness behavior in animals within 1 h of administration.” The behavioral paradigm “was assessed by open field test, forced swim test, and tail suspension test. Further, tumor necrosis factor-α (TNF-α), antioxidant enzymes, and lipid peroxidation were measured in the brain to correlate neuroinflammation and oxidative stress with sickness behavior.”

Both treatments, PI (20 mg/kg) and imipramine (15 mg/kg), were administered orally (once for acute and once daily for 7-day protocols).


Delta Extrax


Researchers found that :LPS elevated the brain TNF-α level, augmented oxidative stress, and induced the sickness behavior in mice. Acute and 7-day treatment of mice with PI significantly reduced the LPS-induced sickness behavior. In addition, PI inhibited the neuroinflammation evidenced by a reduction in brain TNF-α and oxidative stress.”

They conclude by stating that “Our data propose that acute and long-term activation of CB2R might prevent neuroinflammation and oxidative stress-associated sickness behavior.”

For more information on this study, including its full abstract and a link to its full text, click here.

1 Comment

  • Peter Greene
    January 29, 2019

    Thank you for posting about this study. For the vast majority of people it likely makes little to no sense. When they see the words “sickness behavior” they probably equate it with how an ill person outwardly behaves. Sickness behavior describes how the body reacts to illness. A simple example would be a fever from a bacterial infection. The fever is the body’s sickness behavior in reaction to the infection.

    Systemic inflammation is found in diseases like rheumatoid arthritis, coronary heart disease, stroke, type 2 diabetes, and obesity. It is also found in other diseases little understood by the general public. Neuroinflammation and oxidative stress are hallmarks of Gulf War Illness, Parkinson’s disease and Alzheimer’s disease. Researchers have been searching for something that would safely mitigate or eliminate neuroinflammation and oxidative stress for years. Interrupting the cycle of inflammation is key to helping patients with these diseases.

    Hopefully this research will be duplicated and eventually funded for human research. Speaking as someone dealing with Gulf War Illness I have found a great deal of relief with medical marijuana. It is nice to see there are specific actions in the brain and body that can be succinctly described as being positively affected by components of marijuana

    I know these sort of articles don’t get you a ton of hits but posting news about this sort of science does reach those of us who are grateful to see this sort of information posted. Job well done, Anthony!

Post a Comment