This　study　aimed　to　assess　the　ameliorative　effect　and　mechanisms　of　sulforaphane　(SFN)　on　cadmium　(Cd)induced　hepatotoxicity.　Four　in　vitro　free　radical　scavenging　tests,　HepG2　cell　viability　analysis,　and　cadmium　chloride　(CdCl2)　indeced　liver　injured　mice　mode　were　employed.　SFN　scavenged　the　free　radicals　in　vitro,　and　mitigated　the　oxidative　damages　in　HepG2　cells　incubated　with　SFN　+　CdCl2.　In　mice　models,　SFN　pretreatment　dose-dependently　remarkably　improved　redox　homeostasis,　and　attenuated　the　expressions　of　the　key　liver　inflammatory　factors　(TNF-alpha,　IL-6,　IL-1　beta)　by　CdCl2.　The　pathological　examinations　were　consistent　with　the　above　results.　Moreover,　both　mRNA　and　protein　expression　of　hepatic　nuclear　factor-erythroid　2-related　factor　2　and　hemeoxygenase-1　increased,　while　nuclear　factor-kappa　B　reduced　in　Cd　+　SFN　co-treated　groups.　Taken　together,　this　study　firstly　demonstrated　the　anti-oxidant　and　anti-inflammatory　effects　of　SFN　against　Cd　induced　liver　damages,　which　associated　with　the　modulation　of　intrinsic　Nrf2/ARE　and　NF-kappa　B　pathway.