Therapeutic effects of curcumin on seizure and its mechanisms of action

Epilepsy is a neurological disease that significantly reduces the quality of life in diagnosed individuals. Given the imbalanced release of synaptic energy in the brain, seizures are the main hallmarks of epilepsy disorder. Conventional treatments often fall short in managing symptoms and preventing seizure recurrence. Curcumin has shown potential in seizure management due to its anti-inflammatory, antioxidant, anti-apoptosis, and neuroprotective properties. To gather latest evidence on effects of curcumin in treatment and prevention of seizures, focusing on its mechanisms of action and therapeutic potentials. Clinical, in vivo, and in vitro original studies have been gathered up to August 2024 from valid motor engines including PubMed, Google Scholar, Cochrane Library, and ScienceDirect. Curcumin significantly decreases pro-inflammatory cytokines (IL-6, IL-1β, MCP, TNF-α), while simultaneously increasing anti-inflammatory cytokines (IL-10). It suppresses expression of inflammatory genes and signaling pathways such as COX-2 and NLRP3. Its antioxidant effects are evidenced by the elevation of SOD, CAT, GPx, and GSH, along with reduction of oxidative stress markers (NO, MDA, iNOS, MLK, RIP-1, GFAP). Diminished caspase-3 levels and increased CA1 neuron survival ensure its anti-apoptotic properties. Additionally, curcumin regulates pivotal pathophysiological pathways including AP-1, JNK, c-fos, and c-jun. These actions collectively lead to a reduction in seizure severity, duration, and frequency, with increased seizure latency. Curcumin demonstrated significant therapeutic properties in the management of seizures through its anti-inflammatory, antioxidant, and anti-apoptotic effects. However, its clinical application is limited by bioavailability issues, necessitating further research to optimize delivery methods and confirm efficacy and safety through extensive clinical trials.