Cannabidiol attenuates methamphetamine-induced psychosis via anti-oxidative stress: σ1R-mediated mitochondrial dysfunction as a critical pathway - PubMed
4 days ago
- #Cannabidiol
- #Oxidative Stress
- #Methamphetamine
- Cannabidiol (CBD) shows potential in treating Methamphetamine-induced psychosis (MIP) by reducing oxidative stress and mitochondrial dysfunction.
- The study used both in vitro and in vivo models to assess CBD's effects on METH-induced behaviors and neuronal damage.
- CBD (40 mg/kg) was found to alleviate anxiety-like behaviors and cognitive deficits in mice exposed to METH.
- Network pharmacology identified anti-oxidative stress as a key mechanism through which CBD alleviates MIP.
- CBD reduced neuronal damage, mitochondrial superoxide production, and Ca²⁺ dysregulation in the hippocampus and HT22 cells.
- The neuroprotective effects of CBD were linked to Sigma-1 receptor (σ1R) modulation, confirmed by knockout, overexpression, and binding assays.
- Molecular dynamics simulations and surface plasmon resonance (SPR) confirmed stable binding between CBD and σ1R.
- CBD's therapeutic effects are attributed to attenuating σ1R-mediated mitochondrial oxidative stress and Ca²⁺ overload.