Background: Recent preclinical studies demonstrated the potential antiepileptogenic effect of curcumin. Its molecular pathways in modulating epileptogenesis remain unclear. Objectives: This study investigated the epileptogenic processes induced by kainic acid (KA) and to investigate the antiepileptogenic pathways associated with curcumin therapy. Methods: A single dose of KA 10 mg/kg was used to induce a convulsive status epilepticus in female Wistar rats. After one week of curcumin treatment, gene expression profiling by using microarray was conducted on hippocampal tissues. A set of differential expression changes was determined based on criteria of dual fold change in either direction and p < 0.05, whereas gene annotation and pathway analysis had been performed using Database for Annotation, Visualization and Integrated Discovery software. Results: A number of genes significantly altered in expression during KAinduced epileptogenesis. Inflammation and immune response were the prominent overexpressed processes induced by KA. Genes of cell surface molecule (CD74), cytokines and immune response related genes (IL18, IFNGR1, C3, RT1-BA) were significantly up-regulated. Changes of genes related to cell death and gliosis (NCSTN, CTSH) were also observed in KA-induced epileptogenesis. This study revealed that curcumin modulated the epileptogenic process by up-regulating genes related to antiinflammatory cytokines (IL10RB, CXCL16, and CXCL17) and protecting against cell loss by up-regulating NCSTN. It was also likely to exert neuroprotective effects through the up-regulation of CX3CL1 and CXCL16. Conclusion: This study provides novel insights into the mechanisms of curcumin in epileptic brain, which form the basis for future studies looking into its molecular pathway as an antiepileptogenic agent.
Yow, et al.: Anxiety and Recognition Memory Alteration by CurcuminThe effect of curcumin had been studied on anxiety and recognition memory in kainic acid-induced epilepsy. A single dose of intraperitoneal kainic acid (10 mg/kg) was used to induce status epilepticus in female Wistar rats, followed by respective treatments (vehicle dimethyl sulfoxide 50%, curcumin 100 mg/kg/d or levetiracetam 100 mg/kg/d) on the next day for 7 d, with minimum of six rats per group. The behavioural tests were performed before seizure induction and after treatment. Vehicle-treated epileptic rats showed an increase in anxiety-like behaviours in the open field test, which less observed in the light/dark box test. Levetiracetam-treated epileptic rats exhibited anxiolytic behaviours in both the tests. Curcumin-treated epileptic rats exhibited not much difference in anxiety-like behaviour before and after the treatment in open field test, but exhibited anxiolytic behaviours in light/dark box test. Kainic acid impaired the both spatial and non-spatial recognition memories of the rats. Curcumin treatment showed reversal in the non-spatial recognition impaired by kainic acid. In conclusion, kainic acid increases anxiety-like behaviours and impaired recognition memories during the early phase of epileptogenesis and curcumin was potentially improved anxiety and non-spatial recognition memory impaired by kainic acid. These benefits highlighted the potential effect of curcumin to improve psychiatric disorders in epilepsy.
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