| Objective Presently, ischemia reperfusion injury(IRI)is one of the key factors that leads to acute renal failure(ARF) and influences early function of transplanted organ. The mechanism is that many associated factors cause serious injury of ischemic tissues following reperfusion. The recent major aim is to search for the anti-injury substance to prevent IRI directly against the damage or injury of IRI. A number of studies have proved that IRI is related to many factors, such as oxygen free radicals(OFRs), calcium overload, injury of microvessel, action of leucocyte, et al, whereas OFRs is one of the main factors hi the process of IRI. Some studies have demonstrated that antioxidant plays an important role in ameliorating IRI either hi vitro or in vivo for human or animal, and to furthermore investigate the mechanism of IRI is of significance.Heme oxygenase-1 (HO-1) is the rate-limiting enzyme in the conversion of heme into biliverdin, carbon monoxide and free iron. Biliverdin is subsequently reduced to bilirubin, an antioxidant, by biliverdin reductase. Induction of HO-1 occurs as an adaptive and protective response to oxidative stress. In this study, rat renal IRI model was used to further examine the role of HO-1 in cellular defense mechanisms, and specifically to investigate whether prior induction of HO-1 with stannouschloride( SnCb) afifects the subsequent renal IRI in rats.Methods Rat renal ischemic reperfusion model was established. The animals were divided into sham-operation(A), SnCb (B), control (C) and experimental(D) group at random. All the animals were subjected to pentobarbital anesthesia (35~40mg/Kg i.H.). In group A, renal pedicle was not clamped and right kidney was removed; In group B, SnCb was injected (100 # l/100g i.H.) 24h before right kidney was removed, left renal pedicle was not clamped; In group C, 0.9% sodium chloride was injected (100 # l/100g i.H.) 24h before right kidney was removed.At the same time, left renal pedicle was clamped for 45 min,and left kidney was removed after 24h reperfusion; In group D, SnCb was injected (100 # 1/100g i.H.) 24h before 45min renal ischemia, the other protocols were same as group C. Expression of HO-1 was detected by immunohistochemistry and double antibody capture ELISA. Structure of the kidney was evaluated by light microscopy and electron micro- scopy. Activity of superoxide dismutase(SOD) and content of malondialdehyde(MDA) in the renal tissues were examined, and the renal function was also assessed by determining the levels of blood urea nitrogen(BUN) and serum creatinine(Cr).Results (1)Content of HO-1 in renal tissue:HO-l expression was very low in group A. HO-1 expression in group C and D were significantly higher than that in group A (P<0.01). HO-1 expression in group D was significantly higher than that in group B and C (P<0.05). (2)Immunohistochemistry:Imrnunohistochemical study showed HO-1 was positive expression in the plasma and surface of cava of renal tubules cells. Tubule cells expressed low levels of HO-1 protein in group B and C,the highest levels of HO-1 were detected in group D, and there is no positive staining in group A. Glomerulus and interstitial cells were not stained. (3)Activity of SOD and content of MDA in renal tissues: Activity of SOD decreased and content of MDA increased in group C and D after IR, there were no significant differences in group D compared with those before IR (P>0.05), but significant differences existed in group C (P<0.05). Declination of activity of SOD and increase of content of MDA were significant in group C after IR compared with group A (P<0.05 ), whereas there wereno significant difference in group D compared with group A (P > 0.05) . (4) Histopathological changes: Normal morphology was observed by light microscopy in group A and B. Red blood cells in glomerulus were seen and swelling cells of renal tubules appeared without inflammatory cell infiltrated and necrosis foci in group C. Only red blood cells in glomerulus were seen hi group D. (5)Ultrastructure: Normal ult...
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