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Objective To investigate the application of curcumin (Curcumin, CMN) whether induced expression in the body intrarenal heme oxygenase -1 (Heme Oxygenase-1, HO-1), and take this effectively prevent CIN (Contrast-induced The role of nephropathy, CIN). Methods 4-month-old male SD rats to 24, were randomly divided into a control group (A), pure diatrizoate group (B), the diatrizoate CMN group (C), the Pan-meglumine CMN zinc protoporphyrin IX (Zinc protoporphyrin IX, ZnPP IX) group (D), each group of rats 6 experimental time for six weeks. The steps are divided into: 1. Establish CIN model. Specific method is: rat first adaptive feeding for one week, under general anesthesia, resection of the right kidney, then common diet for 4 weeks, 6 weeks in addition to the A group was given a normal diet, and the remaining three groups go salt diet for , rats in each group to furosemide 2mg/kg intramuscularly once a day, the sixth week after giving diatrizoate 1h before via the tail vein injection of indomethacin 10mg/kg, and then separating the side of the common carotid artery, B , C, D group 8mL/kg arterial injection of 60% diatrizoate, A group given normal saline, the metabolic cages to collect the head 24h urine line urinary protein excretion and animals were sacrificed after 48h check kidney blood The successful evaluation CIN modeling effect. Drug intervention's impact on the expression of HO-1 and HO-1 vitality. 24 hours before given diatrizoate advance to Group C CMN 30mg/kg intraperitoneal injection once; Group D CMN 30mg/kg ZnPP Ⅸ 7.5mg/kg intraperitoneal injection time; A, B group, C, D group method given the same amount of physiological salt water. In granting diatrizoate 48h after the rats were killed, taking a part of the kidney tissue for the western blotting quantitative expression of HO-1; another part of the kidney tissue as vitality the homogenate determination HO-1, according to HO-1 degradation blood red Pigment Production of bilirubin in principle, by measuring the generation amount of bilirubin in the reaction system in order to represent the HO-1 vitality. HO-1 expression levels and HO-1 activity between compare different groups. 3. Induction and inhibition of CIN and the underlying mechanism of the HO-1 expression. Rats in each group were sacrificed at the end of the experiment, instantly taken by the heart blood of renal function tests. Portion of the kidney tissue was interleukin -6 (Interleukin-6, IL-6), monocyte chemoattractant protein -1 (MCP-1), malondialdehyde (Malondialdehyde, MDA), Bax, Bcl-2 and cell detection of apoptosis index (AI) and other indicators, the indicators compare different intervention methods. Another part of the kidney tissue placed in 10% neutral buffered formalin fixed, paraffin embedded, sliced, hematoxylin-eosin (Hematoxylin and Eosin, HE) staining, light microscopy, comparing different interventions organizational structure of the kidneys impact. Results of a rat the CIN model of success established. Compared with group A, group B serum creatinine (Cr) increased the extent of 2007 \/ mL (44.2umol / L) or a 25% increase compared with baseline. 2 compared with group A, B, C, D group increased HO-1 expression were. B, C, D group comparison in group C of HO-1 expression amount and HO-1 vitality are significant with the rise, its corresponding kidney damage degree of the significant forward to mitigate; Group D HO-1 expression amount, although group B considerable but HO-1 viability was significantly reduced, and its corresponding degree of kidney damage is significantly heavier. Comparison of 3 groups between IL-6, MDA, MCP-1, Bax, Bcl-2 and AI and other indicators. B, C, D group than in group A were significantly changed. Comparison between groups B, C, D Group C application CMN IL-6, MDA, MCP-1, Bax and AI was significantly lower than that in group B (all P lt; 0.05), Bcl-2 was significantly higher than Group B (all P lt; 0.05); while Group D plus ZnPP Ⅸ IL-6, MDA, MCP-1, Bax and AI was significantly higher than that in group B (all P lt; 0.05), Bcl-2 significantly lower than in group B (all P lt; 0.05). Conclusion 1. Went to a single kidney go the salt diet furosemide indomethacin diatrizoate rat CIN model. 2.CMN can significantly induced HO-1 expression in rat kidney and increase vitality HO-1, but this induction can be ZnPP Ⅸ blocking. 3.CMN anti CIN role may be mediated mainly through the induction of HO-1 expression. 4 anti-inflammatory and oxidative stress, inhibit apoptosis HO-1 renal protection mechanisms.
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