OBJECTIVETo explore the effect of curcumin (CMN) on contrast-induced nephropathy (CIN) in rats and explore the potential mechanisms focusing on heme oxygenase-1 (HO-1) expression.

METHODSMale SD rats (n = 24) were randomly divided into four groups (n = 6 each): control group (group A), diatrizoate group (DTZ, group B), DTZ + CMN group (group C), DTZ + CMN + zinc protoporphyrin IX group (group D). All rats were fed with normal chow for 1 week, right kidney was excised under anesthesia and rats were fed with normal chow for another 4 weeks. Afterwards, rats in group A was fed with normal chow, and rats in group B to D were fed with low-salt diet. All rats were injected furosemide 2 mg×kg(-1)×d(-1) for 7 days intramuscularly. At the beginning of the 7(th) day, rats in group C were injected intramuscularly with CMN 20 mg/kg, rats in group D were injected with CMN (20 mg/kg) + zinc protoporphyrin IX (7.5 mg/kg) while rats in group A and B were injected with equal volume of physiological saline. At the end of the 7(th) day, indometacin (10 mg/kg) was injected into tail vein of all rats. One hour later, 60% DTZ (8 ml/kg) was injected to rats in the group B, C and D while equal volume saline was injected to rats in group A through common carotid artery. After 48 hours, blood was drawn from the hearts of deeply anesthetized rats and kidney tissue was obtained for histology, HO-1, Bax, Bcl-2 expression and the apoptotic index measurements.

RESULTSThe serum creatinine of group B, C and D [(83.67 ± 4.50) µmol/L, (63.67 ± 4.76) µmol/L, (104.17 ± 4.58) µmol/L] was significantly higher than that of group A [(41.50 ± 5.58) µmol/L, all P < 0.05], the serum creatinine was significantly higher in group B than in group C and lower than in group D (all P < 0.05). HO-1 expression of group B, C and D was significantly higher than that of group A (all P < 0.05), significantly higher in group C than in group B and D (all P < 0.05). HO-1 activity of group A, B and C was significantly higher than that of group D(all P < 0.05), HO-1 activity was significantly higher in group B than in group A and significantly lower in group B than in group C (all P < 0.05). Bax, Bcl-2 expression and apoptosis index of group B, C and D were significantly higher than that of group A (all P < 0.05), while Bcl-2/Bax of group B, C and D were significantly lower than that of group A (all P < 0.05). Bcl-2 and Bcl-2/Bax were significantly higher while apoptosis index was significantly lower in group C than in group B (all P < 0.05). Bax and apoptosis index were significantly higher and Bcl-2, Bcl-2/Bax were significantly lower in group D than in group B (all P < 0.05).

CONCLUSIONCMN could protect against contrast-induced nephropathy through reducing renal cell apoptosis via upregulating HO-1 expression and activating HO-1 activity in rats.