The　nuclear　factor-kappa　B　(NF-kappa　B)　family　is　crucial　for　regulating　immune　and　inflammatory　responses.　The　activation　of　the　immune　cell　signaling　pathway　usually　activates　NF-kappa　B,　causing　a　protective　immune　response.　NF-kappa　B　can　also　cause　excessive　inflammatory　responses　by　activating　a　cascade　reaction　of　pro-inflammatory　mediators　such　as　cytokines.　In　this　study,　we　used　an　NF-kappa　B　luciferase　reporter　gene　system.　Out　of　more　than　800　compounds　screened,　four　NF-kappa　B　agonists　were　identified　with　strong　activity　at　nontoxic　concentrations.　Subsequently,　the　adjuvant　effect　was　verified　on　mouse　bone　marrow-derived　dendritic　cells　(BMDCs)　and　macrophages　RAW264.7.　It　was　found　that　fostamatinib　(R788)　disodium　increased　the　production　of　IL-6,　IL-12p40,　and　TNF-alpha,　indicating　that　R788　disodium　could　induce　the　maturation　of　antigen-presenting　cells　(APCs).　In　addition,　three　compounds　were　screened　to　significantly　inhibit　NF-kappa　B　at　nontoxic　doses,　including　dehydrocostus　lactone　(DHL)-a　known　NF-kappa　B　inhibitor.　The　results　showed　that　DHL　significantly　reduced　the　release　of　LPS-induced　inflammatory　cytokines　(including　TNF-alpha,　IL-6,　and　IL-12).　Our　findings　indicate　that　the　NF-kappa　B-based　high-throughput　screening　can　be　used　to　discover　potential　immune　adjuvants　and　anti-inflammatory　molecules.