Arctigenin　(ATG)　is　one　of　the　main　active　substances　in　fruit　derived　from　Arctium　lappa　L.　Previous　studies　have　reported　that　ATG　have　antitumor,　neuroprotective,　antioxidant,　antifibrosis　and　anti-inflammatory　functions.　However,　the　actions　of　ATG　in　kidney　with　acute　injury　following　ischemia/reperfusion　(I/R)　is　still　uncertain.　In　our　study,　mice　were　subjected　to　kidney　I/R　by　having　the　kidney　pedicles　clamped　and　administered　with　vehicle　or　ATG　(1,　3　or　9　mg/kg/d)　via　oral　gavage　for　7　consecutive　days　prior　to　I/R.　Notably,　ATG　aggravated　kidney　I/R　injury　with　the　concentration　increases.　Multiple　biochemical　assays　and　histological　examination　showed　ATG　significantly　alleviated　the　inflammatory　response　as　reflected　by　a　decreased　expression　of　proinflammatory　cytokine,　TLR4/MyD88,　and　NF-kappa　B,　along　with　the　infiltration　of　CD68(+)　macrophage　and　CD11b(+)Gr1(+)　neutrophil　in　the　kidneys.　Meanwhile,　ATG　alleviated　I/R-induced　oxidative　stress　proved　by　increasing　kidney　manganese　superoxide　dismutase　and　glutathione　peroxidase　activity　but　reducing　levels　of　malonaldehyde　and　inducible　nitric　oxide　synthase.　On　the　contrary,　apoptosis　was　significantly　increased　in　kidneys　of　ATG-treated　mice　compared　with　vehicle-treated　controls,　especially　in　tubular　cells.　There　were　increased　numbers　of　TUNEL　positive　cells　and　increased　Bcl-2,　Bax,　cleaved-caspase-3,　and　cleaved-caspase-9　expression.　The　current　study　demonstrates　that　pretreatment　of　ATG　aggravates　I/R　induced　acute　kidney　injury　by　increasing　apoptosis　of　tubular　cells　despite　reducing　infiltrating　inflammatory　cells　and　proinflammatory　cytokine.