Effect of ozone oxidative preconditioning on oxidative stress injury in a rat model of kidney transplantation.

The aim of the present study was to investigate the protective effect of ozone oxidative preconditioning (OOP) on renal oxidative stress injury in a rat model of kidney transplantation. Thirty-six male Sprague Dawley (SD) rats were randomly divided into three groups: A sham (S) group, a kidney transplantation (KT) group and an OOP and kidney transplantation (OOP+KT) group. In the S group, the rats' abdomens were opened and closed without transplantation. In the KT group, the rats received a left kidney from donor SD rats. In the OOP+KT group, donor SD rats received 15 OOP treatments by transrectal insufflations (1 mg/kg), once a day, at an ozone concentration of 50 µg/ml, before the kidney transplantation. Twenty-four hours after transplantation, the parameters of renal function of the recipients were measured. The morphology and pathological effects of renal allograft were examined using hematoxylin and eosin staining, periodic acid-Schiff staining, a terminal deoxynucleotidyl transferase dUTP nick end labeling assay and immunohistochemistry. Markers of oxidative stress were also detected using the thiobarbituric acid method, and expression levels of Nrf-2 and HO-1 were determined by western blot analysis. Blood urea nitrogen and creatinine levels were significantly decreased in the OOP+KT group compared with the KT group, and the morphology and pathological changes of renal allograft were also less severe. Meanwhile, the renal allograft cell apoptosis index was significantly higher in the KT group compared to the OOP+KT group (P<0.05). Levels of superoxide dismutase, glutathione and catalase in the renal allografts were significantly higher in the OOP+KT group compared to those in the KT group (P<0.05), while malondialdehyde levels were significantly lower in the OOP+KT group compared to those in the KT group (P<0.05). Western blot analysis indicated that the expression levels of nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1) were significantly higher in the OOP+KT compared to the KT group (P<0.05). In conclusion, the mechanism by which OOP alleviates oxidative stress injury in renal transplantation may be related to the activation of the signaling pathways of Nrf-2/HO-1 and inhibition of renal tubular epithelial cell apoptosis.

Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model.

PURPOSE: To investigate the potential effects of pretreatment with allopurinol on renal ischemia/reperfusion injury (IRI) in a rat model. METHODS: Twenty four rats were subjected to right kidney uninephrectomy were randomly distributed into the following three groups (n=8): Group A (sham-operated group); Group B (ischemic group) with 30 min of renal ischemia after surgery; and Group C (allopurinol + ischemia group) pretreated with allopurinol at 50 mg/kg for 14 days. At 72 h after renal reperfusion, the kidney was harvested to assess inflammation and apoptosis. RESULTS: Pretreatment with allopurinol significantly improved renal functional and histological grade scores following I/R injury (p<0.05). Compared with Group B, the expression levels of caspase-3 and Bax were markedly reduced in Group C, meanwhile, whereas expression of bcl-2 was clearly increased (p<0.05). A newly described marker of inflammation, High Mobility Group Box 1(HMGB1), showed reduced expression in Group C (p<0.05). CONCLUSION: Pretreatment with allopurinol had a protective effect on kidney ischemia/reperfusion injury, which might be related to the inhibition of HMGB1 expression.

Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

ABSTRACT PURPOSE: To investigate the potential effects of pretreatment with allopurinol on renal ischemia/reperfusion injury (IRI) in a rat model. METHODS: Twenty four rats were subjected to right kidney uninephrectomy were randomly distributed into the following three groups (n=8): Group A (sham-operated group); Group B (ischemic group) with 30 min of renal ischemia after surgery; and Group C (allopurinol + ischemia group) pretreated with allopurinol at 50 mg/kg for 14 days. At 72 h after renal reperfusion, the kidney was harvested to assess inflammation and apoptosis. RESULTS: Pretreatment with allopurinol significantly improved renal functional and histological grade scores following I/R injury (p<0.05). Compared with Group B, the expression levels of caspase-3 and Bax were markedly reduced in Group C, meanwhile, whereas expression of bcl-2 was clearly increased (p<0.05). A newly described marker of inflammation, High Mobility Group Box 1(HMGB1), showed reduced expression in Group C (p<0.05). CONCLUSION: Pretreatment with allopurinol had a protective effect on kidney ischemia/reperfusion injury, which might be related to the inhibition of HMGB1 expression.

Tripterysium glycosides preconditioning attenuates renal ischemia/reperfusion injury in a rat model.

BACKGROUND: Ischemia-reperfusion (I/R) injury to the kidney occurs commonly in organ transplantation from donation after cardiac death, involving many pathologic processes. In this study, we used rat model to assess whether tripterysium glycosides (TG) preconditioning could exert protective effects in renal I/R injury. MATERIALS AND METHODS: All male SD rats were randomly divided into four groups (6 each): sham group, TG group, I/R group and TG + I/R group. Groups TG and TG + I/R were pretreated with TG at 0.1 mg/kg for 14 days; groups sham and I/R were administered with the same dosage of normal saline. Groups TG + I/R and I/R underwent 45 min of renal ischemia of left kidney after right nephrectomy, and then, they were subjected to 72-h reperfusion. Groups sham and TG were only received right nephrectomy. The indicators of apoptosis, fibrosis and inflammation were analyzed to evaluate the effect of tripterysium glycosides preconditioning on renal I/R injury. RESULTS: Pretreatment with TG significantly inhibited the levels of serum creatine and blood urea nitrogen and improved histologic lesions induced by I/R injury. Moreover, for the apoptosis signal pathway, pretreatment with TG markedly decreased the expression of caspase-3 and Bax and increased the level of Bcl-2. HMGB1, which was regarded as one of inflammation marker molecule, it was inhibited in the TG + I/R group. For the fibrosis signal pathway, the pretreatment with TG before I/R could down-regulate the expression level of typical molecules of fibrosis (TGF-ß1, Smad3, p-Smad3). CONCLUSIONS: Pretreatment with tripterysium glycosides exhibited protective effect on kidney ischemia/reperfusion injury, which might be related to the alleviation of inflammation, fibrosis and the reduction in apoptosis.

The effects of artery-ligating and artery-preserving varicocelectomy on the ipsilateral testes in rats.

OBJECTIVES: To investigate the effects of artery-ligating varicocelectomy (ALV) and artery-preserving varicocelectomy (APV) on the ipsilateral testes in experimental varicocele (EV) rats. METHODS: Fifty adolescent male Sprague-Dawley rats (6 weeks old, weighing 170 +/- 10 g) were randomly divided into 4 groups: EV without treatment group (EV group), EV with ALV group (EV+ALV group), EV with APV group (EV+APV group), and a control group. EV was induced by partial ligation of the left renal vein to an external diameter of 50% of its original at the position of medialis to both the adrenal and internal spermatic veins. ALV was performed by total ligation of the dilated left internal spermatic vein, along with the internal spermatic artery. APV was performed by ligation of the dilated left internal spermatic vein only. Johnsen's score, ultrastructure of seminiferous tubules, and intratesticular testosterone concentration (ITC) of the left testes were measured. RESULTS: ITC and Johnsen's score in the control group were significantly higher than those in the EV group (P < .05) and markedly higher than those in the EV+ALV group (P < .01), and no statistical difference compared with those in the EV+APV group (P > .05). Ultrastructural abnormalities of seminiferous tubules were observed in the EV group, especially in the EV+ALV group. CONCLUSIONS: APV was able to repair the varicocele-induced lesions of ipsilateral testes; whereas, the ALV caused further lesions.