The mean ± S.E. was determined for each treatment group. Differences between means were determined with a parametric analysis of variance. When significant differences were detected, treatment groups were compared to the appropriate control using Dunnett’s two-tailed t test. Following a two-way analysis of variance, all groups were compared using Bonferroni’s test. A two-tailed t test was used to determine statistical significance between stimulated groups in the anti-sRBC IgM AFC response between C57BL/6 and CB1 -/- /CB2 -/- mice. Statistical analyses were performed using GraphPad Prism version 4.0a for Macintosh OS X, GraphPad Software (San Diego, CA).
The profile with which CBD targeted T cell cytokine production and proliferation was very similar to that previously reported for two other plant-derived cannabinoid compounds, THC and CBN [18, 19]. These results suggest that the mechanisms by which these three plant-derived cannabinoid compounds suppress cytokine production, at least in vitro, is similar and does not require CB1 or CB2. However, CBD only modestly suppressed the in vivo anti-sRBC IgM AFC response. These data support previous studies conducted in male CD-1 mice in which CBD (≤ 25 mg/kg) did not suppress the in vivo anti-sRBC IgM AFC response . With the demonstration that CBD is efficacious in vivo in a variety of model systems [6, 7, 15, 42], these results suggest that the AFC response in vivo is rather refractory to inhibition by CBD. One explanation for the absence of suppression of the in vivo AFC response is that CBD might be rapidly metabolized in vivo to a non-functional metabolite, particularly because CBD was administered orally. The discrepancy between CBD and THC in vivo versus in vitro does implicate the involvement of one or both cannabinoid receptors in the anti-sRBC IgM AFC response. Further evidence of the requirement for CB1 and/or CB2 in the in vivo anti-sRBC IgM AFC is provided by our observations that the THC-induced suppression of this response was abolished in CB1 -/- /CB2 -/- mice (Springs, et. al., submitted for publication), suggesting that cannabinoids must possess affinity for either CB1 or CB2 to suppress the AFC response in vivo.
2.9 Transient transfections
Splenocytes (2 × 10 5 cells) were treated with CBD (0.2-20 μM) for 30 min at 37°C, followed by cellular activation in complete medium containing 2% (48 hr cultures) or 5% (72 hr cultures) BCS in 96-well culture plates at 0.2 ml/well. Cells were activated with either 40 nM/0.5 μM PMA/Io, 100 ng immobilized anti-CD3 plus 1 μg/ml soluble anti-CD28, or 10 μg/ml lipopolysaccharide (LPS). Splenocytes that were activated with LPS were cultured for 72 hr; splenocytes that were activated with PMA/Io or anti-CD3/CD28 were cultured for 48 hr. Cultures were pulsed with 1 μCi/well of [ 3 H]-thymidine 18 hr prior to harvest, and the cells were harvested onto glass fiber filters using a PHD cell harvester (Cambridge Technology, Inc., Watertown, MA). Tritium incorporation was measured using a Packard Tri-Carb 2100TR Liquid Scintillation Analyzer (Packard Biosciences/Perkin-Elmer, Wellesley, MA).
We also attempted to discern the role of CB1 and CB2 in CBD-induced suppression of the in vitro anti-sRBC IgM AFC response using splenocytes derived from CB1 -/- /CB2 -/- mice. Interestingly, the control anti-sRBC IgM AFC response by splenocytes isolated from CB1 -/- /CB2 -/- mice was remarkably low as compared to that observed with splenocytes isolated from wild type C57BL/6 mice, which limited our ability to absolutely conclude whether CB1 and/or CB2 played a critical role in CBD-induced suppression of the in vitro anti-sRBC IgM AFC response. However, upon examination of the data as percent of vehicle control, it appears unlikely that CB1 and/or CB2 are involved. Although there was a difference between genotypes at lower concentrations of CBD, the response was highly variable, which is likely related to the degree to which the CB1 -/- /CB2 -/- cells were stimulated in vitro with sRBC.
3.4 CBD suppressed the T cell-dependent AFC response
Cannabinoids are a group of structurally-related compounds derived from the Cannabis Sativa plant, which is commonly known as marijuana. The primary psychoactive congener in marijuana is tetrahydrocannabinol (THC) . Although THC is currently approved for medical use as Marinol ® , there exists an ongoing debate in the United States as to whether smoking crude marijuana could be a medical necessity. This debate has sparked interest in determining the physiological properties of some of the other plant-derived cannabinoid compounds. One such compound is cannabidiol (CBD), which is one of the most abundant cannabinoids in the plant.
Standard drug tests don’t screen for CBD because it’s not an intoxicating substance, nor is it an illegal controlled substance. However, some CBD products contain trace amounts of THC, which can affect the results of a drug test.
A growing body of research suggests CBD oil can benefit people with:
As of 2022, CBD that comes from hemp (a type of cannabis sativa plant) that produces no more than 0.3% THC by dry weight is considered legal at the federal level. State laws vary, so it’s best to confirm any rules and regulations that apply to your area with your local and state legislation.
We considered a standard serving size to be 1 milliliter of CBD oil but provided CBD contents per drop as well for people experimenting to find their ideal dose. We evaluated 30-milliliter bottles when possible to keep all data comparable.
Who should use CBD oil?
We then ranked CBD oils based on price, potency, dietary friendliness and flavor options available. Dietary friendliness means we considered the quality of the carrier oil used and whether the product is vegan and gluten-free.