The　study　examined　curcumin＇s　impart　on　relieving　neuroinflammation　of　juvenile　rats　in　kainic　acid　(KA)　induced　epileptic　seizures　by　inhibiting　the　TLR4/MyD88/NF-kappa　B　pathway.　There　were　five　groups:　control,　KA,　KA　+　curcumin　(KC),　KA　+　oxcarbazepine　(OXC)　(KO),　KA　+　curcumin　+　OXC　(KCO)　groups.　KA　was　stereotactically　injected　into　right　hippocampus　following　intraperitoneal　injection　of　curcumin　or　(and)　OXC　for　seven　days.　The　rats　in　the　above　groups　were　randomly　divided　into　three　subgroups　(at　6　h,　24　h,　and　72　h　of　KA　administration)　following　the　seizure　degree　assessed.　The　number　of　NeuN　(+)　neurons　and　GFAP　(+)　astrocytes　was　counted.　The　gene　and　protein　levels　of　TLR4,　MyD88,　and　NF-kappa　B　were　detected.　Compared　with　the　KA　group,　the　seizure　latency　was　longer,　and　the　incidence　of　status　epilepticus　(SE)　was　lower　in　the　KC,　KO,　and　KCO　groups.　The　most　significant　changes　were　in　the　KCO　group.　At　72　h　following　KA　injected,　the　number　of　neurons　was　the　least,　and　the　number　of　astrocytes　was　the　most　in　the　KA　group.　The　number　of　neurons　was　the　most　and　the　number　of　astrocytes　was　the　least　in　the　KCO　group.　At　24　h,　the　mRNA　and　protein　levels　of　TLR4,　MyD88,　and　NF-kappa　B　in　the　KA　group　were　the　most.　The　above　valves　were　the　least　in　the　KCO　group.　Therefore,　curcumin　could　enhance　anti-epileptic　effect　of　OXC,　protect　injured　neurons　and　reduce　proliferated　glial　cells　of　the　hippocampus　of　epileptic　rats　by　inhibiting　inflammation　via　the　TLR4/MyD88/NF-kappa　B　pathway.