CBD and THC and their Neuroprotective Antioxidant Abilities | cannabisMD

CBD and THC and their Neuroprotective Antioxidant Abilities

CBD and THC and their Neuroprotective Antioxidant Abilities; PNAS


Cannabinoids are a collection of over 100 chemical compounds that are derived from the cannabis plant (cannabis sativa). Cannabis is used to treat chronic pain in the United States and clinical trials have shown it could have neuroprotective effects on nerve cells. though Cannabidiol (CBD) is one of these chemicals and research has said it has anti inflammatory effects when induced on animal cells, without unwanted psychoactive side effects. CBD oil is a product derived from cannabis extract and the side effects of CBD are said to be minimal. Tetrahydrocannabinol (THC) is another one of these chemicals that gives off a psychotropic effect in animals brains. CBD and THC are the main components of cannabis. Endogenous cannabinoid receptors (CB1 and CB2) are found in the endocannabinoid system and allow cannabinoids to bind and work in the body. Cannabinoid types in marijuana are known to exert behavioral and psychoactive effects but also to hold therapeutic properties. This paper evaluates another potential therapeutic role for cannabinoids as neuroprotectants and illustrates their mechanism of action in rat cortical neuronal cultures.

Here is the full scientific article if you wish to download it.

Main Points

  • Cannabis could be used as a therapeutic agent
  • THC and CBD are potent antioxidants

Cannabis could be used as a therapeutic agent

The neuroprotective actions of cannabidiol and other cannabinoids were examined in rat cortical neuron cultures exposed to toxic levels of the excitatory neurotransmitter glutamate. Glutamate toxicity was reduced by both cannabidiol, a non psychoactive constituent of marijuana, and the psychotropic cannabinoid tetrahydrocannabinol (THC). The neuroprotection observed with cannabidiol and THC was unaffected by cannabinoid receptor antagonist, indicating it to be cannabinoid receptor independent. Previous studies have shown that glutamate toxicity may be prevented by antioxidants. Cannabidiol, THC and several synthetic cannabinoids all were demonstrated to be antioxidants. Cannabidiol and THC also were shown to stop oxidative damage as well as or better than any other antioxidants in a chemical (Fenton reaction) system and neuronal cultures. This data also suggests that cbd products may be a potentially useful therapeutic drug for the treatment of oxidative neurological disorders such as cerebral ischemia.

THC and CBD are potent antioxidants

During an ischemic episode, large amounts of the excitatory neurotransmitter glutamate are released. Cannabinoids like tetrahydrocannabinol (THC) and its psychoactive components also have been said to be neuroprotective against glutamate toxicity. Cannabinoids have been suggested to prevent glutamate neurotoxicity by triggering cannabinoid receptors. A synthetic cannabinoid (HU-211) also has been seen to be neuroprotective even though it does not trigger cannabinoid receptors. This compound is a normal cannabinoid, however, in that it, unlike other cannabinoids, it possesses some antioxidant abilities. The present study evaluates classical cannabinoids as neuroprotectants but focuses on the nonpsychoactive cannabinoid cannabidiol. Like THC, cannabidiol is a natural part of the marijuana plant, Cannabis sativa, although unlike THC, cannabidiol does not trigger cannabinoid receptors and does not bestow any psychoactive effects. This study demonstrates that cannabidiol and other cannabinoids such as THC are potent antioxidants that protect neurons from glutamate-induced death without cannabinoid receptor activation.


The non psychotropic cannabis compound cannabidiol was found to stop both glutamate neurotoxicity and cell death. The psychotropic effects THC were limited, and also blocked glutamate neurotoxicity with a parallel potency to cannabidiol. In both cases, neuroprotection was not impacted by cannabinoids. This suggests that cannabinoids may have potentially useful analgesic effects that are independent of psychoactivity-inducing cannabinoid receptors and so are not necessarily accompanied by psychotropic side effects in the central nervous system.

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