caryophyllene and Neurogenic-Inflammation

(-)-β-caryophyllene (BCP), a cannabinoid receptor type 2 (CB2)-selective phytocannabinoid, has already been shown in precedent literature to exhibit both anti-inflammatory and analgesic effects in mouse models of inflammatory and neuropathic pain. Herein, we endeavored to investigate the therapeutic potential of BCP on experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). Furthermore, we sought to demonstrate some of the mechanisms that underlie the modulation BCP exerts on autoimmune activated T cells, the pro-inflammatory scenery of the central nervous system (CNS), and demyelination. Our findings demonstrate that BCP significantly ameliorates both the clinical and pathological parameters of EAE. In addition, data hereby presented indicates that mechanisms underlying BCP immunomodulatory effect seems to be linked to its ability to inhibit microglial cells, CD4+ and CD8+ T lymphocytes, as well as protein expression of pro-inflammatory cytokines. Furthermore, it diminished axonal demyelination and modulated Th1/Treg immune balance through the activation of CB2 receptor. Altogether, our study represents significant implications for clinical research and strongly supports the effectiveness of BCP as a novel molecule to target in the development of effective therapeutic agents for MS.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Cannabinoid Receptor Agonists; Cytokines; Demyelinating Diseases; Disease Models, Animal; Encephalomyelitis, Autoimmune, Experimental; Female; Humans; Hyperalgesia; Mice, Inbred C57BL; Microglia; Multiple Sclerosis; Neurogenic Inflammation; Paralysis; Polycyclic Sesquiterpenes; Receptor, Cannabinoid, CB2; Sesquiterpenes; T-Lymphocytes; T-Lymphocytes, Regulatory; Th1 Cells

Amyloid β (Aβ) is the major component of senile plaques (SP) in the brains of Alzheimer's disease (AD) patients, and serves as an inflammatory stimulus for microglia. Trans-caryophyllene (TC), a major component in the essential oils derived from various species of medicinal plants, has displayed its neuro-protective effects in previous studies. However, whether TC has a protective role in AD remains unknown. In this study, the effects of TC on Aβ

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cell Line; Cyclooxygenase 2; Cytokines; Dinoprostone; Humans; Microglia; Neurogenic Inflammation; Nitric Oxide; Nitric Oxide Synthase Type II; Phosphorylation; Polycyclic Sesquiterpenes; Rats; Sesquiterpenes; Toll-Like Receptor 4