Sepsis-induced　acute　kidney　injury　(AKI)　with　high　incidence　and　mortality　rates　remains　a　great　challenge　in　the　clinic;　thus,　novel　therapies　need　to　be　developed　urgently.　This　complication　is　associated　with　an　overwhelming　systemic　inflammatory　response.　The　aim　of　this　study　was　to　evaluate　the　potential　effects　and　possible　mechanisms　of　gold　clusters　on　septic　AKI　in　vitro.　Rat　mesangial　HBZY-1　cells　were　treated　with　peptide-templated　gold　clusters　under　lipopolysaccharide　(LPS)　stimulation.　The　LPS-induced　expression　of　pro-inflammatory　cytokines　was　measured,　including　tumor　necrosis　factor　alpha　(TNF-alpha),　interleukin-1　beta　(IL-1　beta)　and　interleukin-6　(IL-6).　Our　data　showed　that　the　LPS-induced　transcription　and　secretion　of　these　cytokines　were　suppressed　by　pretreatment　of　gold　clusters　in　a　dose-dependent　manner.　Cyclooxygenase-2　(COX-2)　and　inducible　nitric　oxide　synthase　(iNOS)　also　play　key　roles　in　septic　AKI　and　both　of　them　are　induced　upon　LPS-stimulation　in　mesangial　cells.　Our　results　further　showed　that　pretreatment　with　gold　clusters　dramatically　inhibited　the　LPS-stimulated　transcription　and　expression　of　COX2　and　iNOS,　and　the　subsequent　prostaglandin　E2　(PGE2)　and　nitric　oxide　(NO)　production　in　HBZY-1　cells.　Since　these　factors　are　involved　in　the　NF-kappa　B　pathway　upon　LPS　stimulation,　the　potential　roles　of　gold　clusters　on　the　NF-kappa　B　pathway　were　further　determined.　We　found　that　LPS-induced　NF-kappa　B　activation　was　suppressed　in　gold　clusters-pretreated　HBZY-1　cells.　These　results　demonstrated　that　gold　clusters　can　attenuate　LPS-induced　inflammation　in　mesangial　cells,　probably　via　inhibiting　the　activation　of　the　NF-kappa　B　pathway,　suggesting　a　potential　therapeutic　approach　for　septic　AKI.