The NLRP3 inflammasome: a vital player in inflammation and mediating the anti-inflammatory effect of CBD

Chu, Feng-xin; Wang, Xiao; Li, Bo; Xu, Li-li; Di, Bin

doi:10.1007/s00011-023-01831-y

Cited by 5 publications

(1 citation statement)

References 163 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cannabidiol (CBD) is a psychoactive phytocannabinoid devoid of addictive potency, with potential beneficial effects in the treatment of neurological and neuropsychiatric disorders [1][2][3][4][5]. CBD is a multitargeted drug with neuroprotective and anti-inflammatory properties, which shows affinity to various molecular targets, comprising peroxisome proliferator-activated receptor gamma (PPARγ), transient receptor potential vanilloid receptors (TRPV), G protein-coupled receptor 55 (GPR55), 5-HT 1A serotonin receptors, enzymes, transporters and ion channels, and negligible affinity to cannabinoid CB1 and CB2 receptors [6][7][8][9][10]. Furthermore, CBD was reported to interfere with pivotal mechanisms of neuronal death in neurodegenerative disorders such as oxidative stress and excitotoxicity [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Cannabidiol (CBD) against Qxidative Stress, but Not Excitotoxic-Related Neuronal Cell Damage—An In Vitro Study

Jantas,

Leśkiewicz,

Regulska

et al. 2024

Biomolecules

View full text Add to dashboard Cite

Cannabidiol (CBD) appears to possess some neuroprotective properties, but experimental data are still inconsistent. Therefore, this in vitro study aimed to compare the effects of CBD in a wide range of concentrations on oxidative stress and excitotoxic-related cell damage. Results showed that low concentrations of CBD ameliorated the H2O2-evoked cell damage of primary cortical neuronal cell culture. However, higher concentrations of CBD alone (5–25 μM) decreased the viability of cortical neurons in a concentration-dependent manner and aggravated the toxic effects of hydrogen peroxide (H2O2). Neuroprotection mediated by CBD in primary neurons against H2O2 was not associated with a direct influence on ROS production nor inhibition of caspase-3, but we found protective effects of CBD at the level of mitochondrial membrane potential and DNA fragmentation. However, CBD had no protective effect on the glutamate-induced cell damage of cortical neurons, and in higher concentrations, it enhanced the toxic effects of this cell-damaging factor. Likewise, CBD, depending on its concentration, at least did not affect or even enhance cortical cellular damage exposed to oxygen–glucose deprivation (OGD). Finally, we showed that CBD in submicromolar or low micromolar concentrations significantly protected human neuronal-like SH-SY5Y cells against H2O2- and 6-hydroxydopamine (6-OHDA)-induced cell damage. Our data indicate that CBD has a dual effect on oxidative stress-induced neuronal death-in low concentrations, it is neuroprotective, but in higher ones, it may display neurotoxic activity. On the other hand, in excitotoxic-related models, CBD was ineffective or enhanced cell damage. Our data support the notion that the neuroprotective effects of CBD strongly depend on its concentration and experimental model of neuronal death.

show abstract