Aims: To investigate the potential role of renalase in adriamycin nephropathy and the effect of lisinopril on the regulation of renalase. Methods: Adriamycin nephropathy was induced in male Wistar rats (n=12) by a single injection of adriamycin at 2 mg/kg body weight. Rats were then randomly assigned to a model group or a treatment group, to which were administered distilled water or the angiotensin converting enzyme inhibitor lisinopril, respectively, for 12 weeks. Six normal rats served as controls. At the end of study, physiological parameters and systolic blood pressure were measured. Glomerulosclerosis and tubulointerstitial injury were assessed by histopathology Renalase protein expression in kidney was quantified by immunohistochemistry and immunoblotting. The serum concentration and urinary excretion of renalase were determined by enzyme-linked immunosorbent assay. Results: In model group rats, proteinuria and systolic blood pressure were elevated. Increased serum renalase concentration was observed; however, renalase protein expression in the kidney was significantly decreased. Compared with the model group, decreased proteinuria, lower systolic blood pressure, and fewer morphologic lesions were detected in the treatment group. Although levels of serum renalase were similar, accumulation of renalase in urine and kidney tissue increased notably in the treatment group compared with the model group. Conclusions: This study suggests that renalase may be involved in the process of adriamycin-induced renal injuries. Lisinopril may attenuate adriamycin-induced kidney injury by controlling blood pressure, which may be partially attributed to the renalase expression and secretion.
To guide the administration of fat emulsion in the nutritional support of acute renal failure (ARF), pharmacokinetic analysis with an one-compartment open model after bolus intravenous injection was performed to compare the elimination kinetics of long-chain triglycerides (LCT) and medium-chain triglycerides (MCT) in ischemic acute renal failure rats. Sprague-Dawley rats were randomized into four groups, namely LCT normal group, LCT ARF group, MCT normal group and MCT ARF group. The model of ischemic acute renal failure was induced by clamping the left renal artery for 60 min and contralateral nephrectomy. All the rats were fasted with water ad libitum for 10 h before 0.3 g/kg body weight of 10% Intralipid (LCT) or 10% Lipofundin (MCT: LCT = 50:50) was injected as a bolus to them via the tail vein. The serum triglyceride concentration was determined at 2, 10, 40, 70, 100, 130 and 160 min after intravenous injection for kinetic analysis. The results showed that the elimination rate constant (ke) of LCT ARF group was significantly decreased, while the half life period (t1/2) of it was significantly longer than those of LCT normal group. The ke and t1/2 of MCT showed no statistical difference between normal and ARF groups. In the normal group the ke of LCT was significantly decreased compared with MCT whereas the t1/2 was significantly prolonged. In the ARF group the ke of LCT was much less than that of MCT while the t1/2 was much longer. The serum insulin levels of both MCT groups were significantly higher than those of LCT groups. These results indicate that MCT will be eliminated more rapidly than LCT in ARF rats. MCT may also increase the secretion of insulin. In conclusion, MCT may be more favorable than LCT in the nutritional management of ARF.
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