Many claim CBD is a more powerful antioxidant than the vitamins C and E. Based on what science has taught us so far, we can assume it. The Powerful Antioxidant Properties of CBD For Your Skin. Tamryn Burgess. Posted on December 19 CBD Skincare. When you think about antioxidants . This study reports that cannabidiol and other cannabinoids such as THC are potent antioxidants that protect neurons from glutamate-induced.
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This study reports that cannabidiol and other cannabinoids such as THC are potent antioxidants that protect neurons from glutamate-induced death without cannabinoid receptor activation.
Cannabidiol, THC, and reagents other than those specifically listed below were purchased from Sigma. Dihydrorhodamine was supplied by Molecular Probes. Tert -butyl hydroperoxide, tetraethylammonium chloride, ferric citrate, and sodium dithionite were all purchased from Aldrich. Solutions of cannabinoids, cyclothiazide, and other lipophiles were prepared by evaporating a 10 mM ethanolic solution under a stream of nitrogen in a siliconized microcentrifuge tube.
After evaporation, 1 ml of culture media was added, and the drug was dispersed by using a high power sonic probe. Special attention was used to ensure the solution did not overheat or generate foam. After dispersal, all solutions were made to their final volume in siliconized glass tubes by mixing with an appropriate quantity of culture media. Primary cortical neuron cultures were prepared according to the method of Ventra et al In brief, fetuses were extracted by C-section from a day pregnant Wistar rat, and the fetal brains were placed into phosphate buffered saline.
Cells were counted, were tested for vitality by using the trypan blue exclusion test, and were seeded onto poly- d -lysine coated 24 multiwell plates. This protocol results in a highly neuron-enriched culture Media were conditioned by 24 hr of treatment over a confluent layer of type I astrocytes prepared from 2-day-old Wistar rat pups In brief, cortices were dissected, were cut into small pieces, were digested enzymatically with 0.
The cell suspension then was plated into untreated cm 2 T-flasks, and, after 24 hr, the media were replaced and unattached cells were removed.
Once astrocytes achieved confluency, cells were divided into four flasks. Astrocyte cultures were used to condition DMEM for no longer than 2 months. After exposure, cells were washed twice with saline and were incubated for 18 hr in conditioned DMEM. Cells were incubated with glutamate in the presence of nM MK for 18—20 hr before analysis. Specific AMPA and kainate receptor ligands also were used to separately examine the effects of cannabinoids on AMPA and kainate receptor-mediated events.
When specifically examining kainate receptor activity, cyclothiazide was replaced with 0. Although the neuron preparation technique described above results in a largely neuronal culture, a minority of astrocytic cells remain. Astrocytes are highly resistant to glutamate toxicity 16 because of their lack of functional NMDAr 17 , 18 , although glutamate toxicity in astrocytes has been observed to prevent AMPA receptor desensitization if cyclothiazide is present It was concluded, therefore, that astrocyte contamination does not contribute substantially to the effects of glutamate in our neuronal cultures.
Tert -butyl hydroperoxide was used because its miscibility with both water and lipids allows oxidation to occur in both cytosolic and membrane-delimited cellular compartments.
Cell toxicity was assessed 18—20 hrs after insult by measuring lactate dehydrogenase release into the phenol red-free culture media. Experiments were conducted with triple or quadruple values at each point, and all plates contained positive glutamate alone and baseline controls. The assay was validated by comparison with a tetrazolium-based viability assay XTT Results were similar with either system, although lactate dehydrogenase release was used in this study because it provided a greater signal to noise ratio than the XTT assay.
Tetraethylammonium chloride in acetonitrile 0. The antioxidant activities of each of the compounds were evaluated by their ability to prevent oxidation of dihydrorhodamine to the fluorescent compound rhodamine. Oxidant was generated by ferrous catalysis diothionite-reduced ferric citrate of tert -butyl hydroperoxide in a Various concentrations of cannabinoids and butylhydroxytoluene BHT were included to examine their ability to prevent dihydrorhodamine oxidation.
Data are reported as mean values plus and minus standard error. To examine NMDAr-mediated toxicity, rat cortical neurons were exposed to glutamate for 10 min in a magnesium-free medium, and the level of lactate dehydrogenase released was used as an index of cell injury. Similar data also was observed when glutamate was replaced with either AMPA-specific or kainate receptor-specific ligands data not shown. Each experiment was repeated on at least four occasions with essentially the same results.
Cannabinoids were present during and, in the case of NMDAr mediated toxicity, after the glutamate exposure periods. See Materials and Methods for further experimental details. Such depolarization may activate both voltage-sensitive calcium channels 21 and facilitate NMDAr activation 22 , However, a combination of these calcium channel inhibitors did not completely block EDTA-preventable calcium-dependant cell death.
Cannabinoids were present throughout the glutamate exposure period. Significant difference between EDTA and other treatments is indicated with an asterisk. Unlike cannabidiol, THC is a ligand for the brain cannabinoid receptor 24 , and this action has been proposed to explain the ability of THC to protect neurons from NMDAr toxicity in vitro 7.
This was confirmed by inclusion of a cannabinoid receptor antagonist, SRA Fig. Neither THC or cannabidiol neuroprotection was affected by cannabinoid receptor antagonist. Effect of THC, cannabidiol, and cannabinoid receptor antagonist on glutamate induced neurotoxicity. See Materials and Methods for experimental details. Studies have suggested that ROS damage may be involved in glutamate neurotoxicity 5 , 6. To investigate whether cannabinoids could protect neurons against glutamate by reacting with ROS, the antioxidant properties of cannabidiol and other cannabinoids were assessed.
Cyclic voltametry, a procedure that measures the ability of a compound to accept or donate electrons under a variable voltage potential, was used to measure the oxidation potentials of several natural and synthetic cannabinoids.
Anandamide arachidonyl-ethanolamide , which is not a cannabinoid in structure but is an endogenous ligand for the cannabinoid receptor, did not undergo oxidation in this assay Fig. Three other cannabinoids, cannabinol, nabilone, and levanantrodol, also were tested, and they, too, exhibited oxidation profiles similar to cannabidiol and THC data not shown.
A A comparison of the oxidation potentials of cannabinoids and the antioxidant BHT. Anandamide, a cannabinoid receptor ligand with a noncannabinoid structure, was used as a nonresponsive control. Experiments were repeated three times with essentially the same results.
B Effect of cannabidiol and THC on dihydrorhodamine oxidation. Cannabinoids were compared with BHT for their ability to prevent tert -butyl hydroperoxide-induced oxidation of dihydrorhodamine. This experiment was repeated four times with essentially the same results. The ability of cannabinoids to be oxidized readily suggests that they may possess antioxidant properties comparable to BHT. These properties were examined further in a Fenton reaction iron-catalyzed ROS generation.
But it's something much more insidious. Free radicals are molecules that are created as waste products when the cells in your body generate energy. At times this can be a good thing, but when those molecules bind with critical molecules in your body, including your DNA, it can cause changes that lead to stress, aging, heart disease, and stroke, just to name a few.
Environmental toxins such as cigarette smoke, chemicals, and smog also cause exposure to free radicals. Here they come to save the day. Antioxidants are mercenary molecules, heroes that are willing to give up their lives to secure your health and well-being. They bind with free radicals, rendering them harmless and preventing them from doing any serious damage. Antioxidants are created naturally in many fruits and veggies such as red beans, chocolate, coffee, spices, berries, nuts, and a host of fruits and vegetables.
Hence the reason you should be eating more of them. As it turns out, CBD is a powerful antioxidant. In fact, CBD is an even more powerful antioxidant than vitamin E, or even vitamin C, which is known as the king of antioxidants. Don't take our word for it.
Like most plants, there are also numerous other antioxidants found in cannabis. But most people don't have the right or the time to grow their own cannabis.
There are many more practical ways take advantage of CBD's antioxidant properties. There are oral applications such as CBD hemp oil. Hemp oil contains a host of antioxidants. There's also the vape option. Rick Schettino - 5 September Let's take a look inside and see what's going on. What are free radicals? Fighting free radicals with antioxidants Fear not! Are there antioxidants in cannabis? So get yourself some CBD and fight those free radicals! Rick Schettino - Jan 12,
CBD Has Antioxidant and Neuroprotective Properties. What Does That Mean?
This study further shows that CBD acts as a powerful antioxidant, able to not only stop various conditions and diseases related to rapid. Anything containing vitamins C and E will give an antioxidant boost, but did you know that the cannabis compound CBD has been found to be just as powerful. THC and CBD are powerful antioxidants—more powerful than vitamin C and About the antioxidant properties of cannabis and cannabinoid.