The other receptor, called CB2, is found in tissues in the rest of the body and triggers a cascade of biochemical reactions that can help combat inflammation.
"Our interest is to exploit the pharmacological nature of the CB2 receptor," because it does not have psychotropic side effects, Gertsch explained in an email.
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"Targeting the CB2 receptor could be a therapeutic strategy to prevent or treat diseases like Crohn's disease [inflammation of the intestinal tract], liver cirrhosis, osteoarthritis, and atherosclerosis."
THC activates both receptors, so it won't alleviate inflammation without also making people high.
But (E)-BCP affects only the CB2 receptor, according to the new study, which appears in today's issue of the Proceedings of the National Academy of Sciences.
As part of their research, the scientists engineered a strain of mice that lacked the CB2 receptor. The team then fed the modified mice and normal mice a diet rich in (E)-BCP.
When the scientists induced inflammation with chemicals, normal mice experienced an anti-inflammatory effect while the genetically engineered mice did not.
"This experiment shows that the anti-inflammatory effects are mediated via the CB2 receptor," Gertsch said.
Drug Building Block?
Stephen Safe, director of the Texas A&M University's Center for Environmental and Genetic Medicine, said he is impressed by the team's results both in mouse cells and in live mice.
"They did a good study," said Safe, who was not involved in the research.
He also noted that a lot of other studies have been finding that fat-soluble chemicals from plants activate many receptors in the body.
"A lot of these [come from plants that] have been used in traditional medicine," he said. "This is another example of that—but a bit of a sexy one."
In this case, he noted, Gertsch's team has identified some "petty good" activators of the CB2 receptor.
"Can they be further developed and modified into better anti-inflammatory drugs?" he asked. "Maybe. [(E)-BCP] could be a new model [compound] for drug design."
