cannabidiol has been researched along with Leukemia* in 2 studies
2 other study(ies) available for cannabidiol and Leukemia
| Article | Year |
|---|---|
Cannabidiol Enhances Intestinal Cannabinoid Receptor Type 2 Receptor Expression and Activation Increasing Regulatory T Cells and Reduces Murine Acute Graft-versus-Host Disease without Interfering with the Graft-versus-Leukemia Response.
Cannabidiol (CBD) is a highly lipidic phytocannabinoid with remarkable anti-inflammatory effects. The aim of this study was to evaluate CBD's effects and mechanisms of action in the treatment of mice subjected to acute graft-versus-host disease (aGVHD). aGVHD was induced by the transplantation of bone marrow cells and splenocytes from C57BL-6j to Balb-c mice. The recipient mice were treated daily with CBD, and the treatment reduced mouse mortality by decreasing inflammation and injury and promoting immune regulation in the jejunum, ileum, and liver. Analysis of the jejunum and ileum showed that CBD treatment reduced the levels of C-C motif chemokine ligand (CCL) 2, CCL3, CCL5, tumor necrosis factor Topics: Animals; Bone Marrow Transplantation; Cannabidiol; Cells, Cultured; Chemokines, CC; Graft vs Host Disease; Interferon-gamma; Intestinal Mucosa; Leukemia; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Receptor, Cannabinoid, CB2; T-Lymphocytes, Regulatory; Tumor Necrosis Factor-alpha | 2021 |
Cannabidiol-induced apoptosis in human leukemia cells: A novel role of cannabidiol in the regulation of p22phox and Nox4 expression.
In the current study, we examined the effects of the nonpsychoactive cannabinoid, cannabidiol, on the induction of apoptosis in leukemia cells. Exposure of leukemia cells to cannabidiol led to cannabinoid receptor 2 (CB2)-mediated reduction in cell viability and induction in apoptosis. Furthermore, cannabidiol treatment led to a significant decrease in tumor burden and an increase in apoptotic tumors in vivo. From a mechanistic standpoint, cannabidiol exposure resulted in activation of caspase-8, caspase-9, and caspase-3, cleavage of poly(ADP-ribose) polymerase, and a decrease in full-length Bid, suggesting possible cross-talk between the intrinsic and extrinsic apoptotic pathways. The role of the mitochondria was further suggested as exposure to cannabidiol led to loss of mitochondrial membrane potential and release of cytochrome c. It is noteworthy that cannabidiol exposure led to an increase in reactive oxygen species (ROS) production as well as an increase in the expression of the NAD(P)H oxidases Nox4 and p22(phox). Furthermore, cannabidiol-induced apoptosis and reactive oxygen species (ROS) levels could be blocked by treatment with the ROS scavengers or the NAD(P)H oxidase inhibitors. Finally, cannabidiol exposure led to a decrease in the levels of p-p38 mitogen-activated protein kinase, which could be blocked by treatment with a CB2-selective antagonist or ROS scavenger. Together, the results from this study reveal that cannabidiol, acting through CB2 and regulation of Nox4 and p22(phox) expression, may be a novel and highly selective treatment for leukemia. Topics: Animals; Apoptosis; Cannabidiol; Caspases; Cell Survival; Cytochromes c; Enzyme Activation; Extracellular Signal-Regulated MAP Kinases; Female; Humans; JNK Mitogen-Activated Protein Kinases; Jurkat Cells; Leukemia; Membrane Potentials; Mice; Mitochondrial Membranes; NADPH Oxidase 4; NADPH Oxidases; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Reactive Oxygen Species; Receptor, Cannabinoid, CB2 | 2006 |