July 22, 2008 Cannabis has long been accredited with anti-inflammatory properties. ETH Zurich researchers, however, have now discovered that it is not only the familiar psychoactive substances that are responsible for this; a compound we take in every day in vegetable nutriment also plays a significant role.
People not only rate cannabis sativa L. highly because of its intoxicating effects; it has also long been used as a medicinal plant. Although the plant has been scrutinized for years, surprising new aspects keep cropping up. For example, researchers from ETH Zurich and Bonn University examined a component in the plant’s essential oil that until then had largely been ignored and found it to have remarkable phar- macological effects. The findings open up interesting perspectives, especially for the prevention and treatment of inflammations.
Completely different molecule structure
The hemp plant contains over 450 different substances, only three of which are responsible for its intoxicating effect. They activate the two receptors in the body CB1 and CB2. Whilst the CB1 receptor in the central nervous system influences perception, the CB2 receptor in the tissue plays a crucial role in inhibiting inflammation. If the receptor is activated, the cell releases fewer pro-inflammatory signal substances, or cytokines. The scientists have now discovered that the substance beta-carophyllene, which composes between 12 and 35 percent of the cannabis plant’s essential oil, activates the CB2 receptor selectively.
Unlike the three psychoactive substances, however, beta-carophyllene does not latch onto the CB1 receptor and consequently does not trigger the intoxicating effect. “Due to the various effects of cannabis, we had suspected for quite some time that other substances could come into play besides the psychoactive ones”, explains Jürg Gertsch from the Institute of Pharmaceutical Sciences at ETH Zurich. “However, astonishingly we didn’t know what substances these were until now.”
Gertsch finds it remarkable that beta-carophyllene has a very different molecule structure to that of the classical cannabinoids. “This is presumably why no one realized that the substance can also activate the CB2 receptor.” The scientists were not only able to prove that beta-carophyllene binds with the CB2 receptor in vitro but also in animal tests, where they treated mice that were suffering from an inflammatory swelling on their paws with orally administered doses of the substance. The swelling declined in up to 70 percent of the animals, even for deep doses. For mice lacking the gene for the CB2 receptor, however, the substance did not make an impact.
The results are encouraging for the prevention or treatment of ailments in which the CB2 receptor plays a positive role. However, Gertsch explains that we are still very much in the early stages on that score. That said, the scientist can conceive that some day the compound will not only help heal certain forms of inflammation, but also be instrumental in treating chronic illnesses, such as liver cirrhosis, Morbus Crohn, osteoarthritis and arteriosclerosis. In all of these diseases, the CB2 receptor and the associated endocannabinoid system play a crucial role.
The beauty is that beta-carophyllene is not only found in cannabis but also often in plants as a whole and we consume the substance in our diet. The non-toxic compound, which incidentally has been used as a food additive for many years, can be found in spice plants like oregano, basil, cinnamon and black pepper. “Whether we have found a new link between the vegetable diet and the prevention of so-called lifestyle diseases in our study remains to be seen in future studies”, adds Gertsch.
Other social bookmarking and sharing tools:
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
- Gertsch et al. Beta-caryophyllene is a dietary cannabinoid. Proceedings of the National Academy of Sciences, 2008; 105 (26): 9099 DOI: 10.1073/pnas.0803601105
Note: If no author is given, the source is cited instead.