Abstract: Objective To explore the relationship between oxidative stress and contrast induced nephropathy (CIN), and observe the effects of hydroxytyrosol on CIN in CIN rats. Methods 84 Wistar rats were randomly divided into 3 groups:Sham-operation group, CIN model group and hydroxytyrosol intervention group. CIN models were prepared for rats in the CIN model group and the hydroxytyrosol intervention group:a indwelling needle was placed in the tail vein of rats; and indomethacin (10 mg/kg),L-NAME (N-nitro-L-arginine methyl ester) (10 mg/kg) and 76% panoplylamine (10 mg/kg) were injected in the same amount every 15 min; in the sham operation group, the same doses of indomethacin,L-NAME and physiological saline were injected with the same method. In the hydroxytyrosol intervention group, hydroxytyrosol (10 mg·kg^-1·d^-1) was administered intragastrical 3 days before and on the day of death; in the Sham-operation group and the CIN model group he same amount of saline was given intragastrical. Rats were sacrificed for collection of tissue and blood samples at 48h after modeling. Serum creatinine (Scr) and Blood urea nitrogen (BUN) were detected and pathological changes of the kidney were evaluated. Apoptosis of tubular cells was detected by TUNEL staining. The contents of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were detected by ELISA. Results No obvious pathological change and apoptosis were found in the sham-operation group. Scr, BUN and the content of MDA in the CIN model group were higher than those in the sham-operation group, the content of SOD and GSH-Px in the CIN model group were significantly lower compared with the sham-operation group (P<0.05). Scr, BUN and the content of MDA in the hydroxytyrosol intervention group were lower and the content of SOD and GSH-Px were significantly higher, compared with the CIN model group. Pathological changes and apoptosis of tubular cells in the intervention group were less serious than those in the model group, but still more serious than the sham-operation group. Conclusions Oxidative stress may be involved in pathogenesis and progression of CIN, and while hydroxytyrosol can protect CIN in rats through alleviating the oxidative stress.