Project description:We used microRNA microarrays to identify dysregulated microRNAs in CD4+ T cells isolated from brains of EAE mice treated with vehicle or THC+CBD.
Project description:Primary glioma stem cells cultured as neurospheres in NBL media with growth factors were subjected to treatment with the non-toxic, non-psychoactive cannabis compound cannabidiol (CBD). Control and CBD- treated cultures were used to generate RNA used to hybridize on Affymetrix DNA arrays Fluorescence intensities data were RMA-normalized using Partek software.
Project description:Increased availability of cannabis and cannabinoid-containing products necessitates the need for understanding how exposure to these compounds can affect development. Using cannabinoid receptor-null zebrafish (cnr1-/- and cnr2-/-), we conducted experiments to assess the roles of these receptors in ∆9-tetrahydrocannabinol (THC) and cannabidiol (CBD) developmental and behavioral toxicity. THC increased mortality and deformities (pericardial and yolk sac edemas, a reduction in size) in cnr1-/- and cnr2-/- fish. Conversely, CBD-induced malformations and mortality were significantly reduced in the cnr1-/- and cnr2-/- larvae. THC and CBD exposure caused significantly decreased larval behavior (96 hpf), however, decreased distance travelled was protected in the cnr1-/- and cnr2-/- fish, suggesting these receptors are responsible for mediating behavioral toxicity. Transcriptomic profiling in cnr+/+ embryos developmentally exposed to 4 μM THC or 0.5 μM CBD revealed that a significant portion of differentially expressed genes were targets of PPARγ, a predicted upstream regulator. In Cnr-positive embryos, co-exposure to the PPARγ inhibitor GW9662 and THC or CBD, there was increased toxicity compared to exposure with THC or CBD alone. Co-treatment in the cnr2-/- fish with GW9662 did not alter the CBD-induced decrease in activity. However, co-treatment with GW9662 did remove the protective effect observed in cnr1-/- fish treated to CBD alone. Collectively, these results indicate that PPARγ, Cnr1, and Cnr2 all play crucial roles in the developmental toxicity of THC and CBD.
Project description:Cannabidiol (CBD) actions in the brain are largely complex and not fully understood. One important brain structure that is a target for CBD, and for which health-beneficial CBD consequences can be seen is the hypothalamus. Given the fundamental role of gene expression in the hypothalamus's regulatory functions, this study undertook the analysis of changes arising in hypothalamic cells’ transcriptomes following various CBD treatments. For this purpose, we used a hypothalamic cellular model, namely we employ adult-derived mHypoA-2/12 mouse cell lines. In the course of the study, the neural cells were treated with different CBD doses (ranging from 0.325 to 3 µM) and vehicle as a control for 6 and 24 hours. The experiment setup allowed us to evaluate both the dosage and time-dependent effect of CBD on hypothalamic cells, particularly on their viability, apoptosis, and transcriptome profile.
Project description:Primary glioma stem cells cultured as neurospheres in NBL media with growth factors were subjected to treatment with the non-toxic, non-psychoactive cannabis compound cannabidiol (CBD). Control and CBD- treated cultures were used to generate RNA used to hybridize on Affymetrix DNA arrays
Project description:Considering reports about positive role of Cannabidiol (CBD) in alcohol abuse disorders, in this study we used cellular model of human fibroblasts to analyse the effect of CBD on ethanol-treated cells. We assumed, that CBD will (to some extent), prevent adverse transcriptional changes driven by alcohol administration and this effect will be detectable on the transcriptome level. As a by-product of this analysis, ethanol and CBD alone stimulated transcriptome changes were also described. We moreover considered that CBD effects are dose and time-dependent. As a model for these analyses we selected human fibroblast cell line as a most abundant cell type in human body that express e.g. both cannabinoid receptors (CB1 and CB2) and is able to metabolize ethanol trough alcohol dehydrogenase activity.