Acute anticonvulsant effects of dapsone on PTZ- and MES-induced seizures in mice: NLRP3 inflammasome inhibition and Nrf2/HO-1 pathway preservation.
Level 5 - mechanism / opinion, no new human data
Animal experimental study
PubMed 39869286 · doi:10.1007/s43440-025-00698-6
What was done
Researchers tested the acute anticonvulsant effects of dapsone (2, 5, 10, and 20 mg/kg, ip) in mice using pentylenetetrazole (PTZ)-induced clonic seizure and maximal electroshock (MES)-induced generalized tonic-clonic seizure models. Effects on oxidative stress and neuroinflammatory markers (Nrf2/HO-1, NLRP3 inflammasome, IL-1β, IL-8, and IL-18) were assessed using Western blotting and ELISA.
What was found
Dapsone (2, 5, 10, and 20 mg/kg) significantly increased the clonic seizure threshold following intravenous PTZ infusion, with doses of 5, 10, and 20 mg/kg increasing latency and decreasing seizure count. In the MES model, dapsone at 10 and 20 mg/kg prevented generalized tonic-clonic seizures and mortality. Dapsone also modulated the Nrf2/HO-1 and NLRP3/IL-1β/IL-18 pathways. Exact quantitative values and effect sizes were not reported in the abstract.
Why it matters
This study provides preclinical evidence that dapsone exerts acute anticonvulsant effects via antioxidant and anti-inflammatory mechanisms in rodent models. It suggests a potential mechanistic basis for further investigation into dapsone-related compounds for drug-resistant epilepsy.
Limits
The study was conducted entirely in mice using acute chemical and electrical seizure models, which do not fully replicate chronic human epilepsy. The abstract omits sample size, numerical data, statistical effect sizes, and assessment of potential toxicity or chronic efficacy.
Cited by
- supports Dapsone penetrates the brain and inhibits NLRP3 inflammasomes.