Acta radiologica (Stockholm, Sweden : 1987) · 2009
The protective role of telmisartan against nephrotoxicity induced by X-ray contrast media in rat model.
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Duan Shao Bin, Wang Yu Hui, Liu Fu You, Xu Xiang Qing, Wang Pian, Zou Qin, Peng You Ming
Аннотация
BACKGROUND: Contrast-induced nephropathy is a serious complication of diagnostic and interventional procedures.
PURPOSE: To evaluate the nephrotoxicity of high- and low-osmolar contrast media (HOCM, LOCM) on kidneys in Sprague-Dawley rats. Telmisartan was administered to confirm its protective role against nephrotoxicity induced by contrast media.
MATERIAL AND METHODS: Sixty male rats were randomly divided into six groups (n=10/group). Glycerin was given to all rats except controls to induce renal injury. HOCM (diatrizoate) or LOCM (iohexol) (10 ml/kg b.w., 300 mg I/ml) was given through a caudal vein. Serum creatinine level was measured by an automatical biochemical analyzer. Caspase-3 activity and Angiotensin II (Ang II) level of renal tissue were detected by fluorometric method and radioimmunoassay, respectively. The renal injury was also assessed by hematoxylin and eosin and TdT-mediated deoxyuridine nick end-labeling staining.
RESULTS: In diatrizoate-injected rats, serum creatinine level was increased (P<0.001). There was no significant difference between iohexol animals and glycerol controls in the level of serum creatinine. The renal caspase-3 activity and Ang II levels in HOCM and LOCM groups were higher than those in glycerol control group (P<0.001). The percentage of apoptotic tubular cells and pathological scores were lower in the iohexol animals than that in the diatrizoate animals (P<0.001). In the groups pretreated with telmisartan, no increase in the levels of serum creatinine, renal Ang II, and caspase-3 activity was observed (P>0.05). The renal injuries induced by contrast media were alleviated.
CONCLUSION: Both HOCM (diatrizoate) and LOCM (iohexol) could cause renal tubular cell apoptosis in the kidneys damaged by glycerin. LOCM was less toxic to rat kidneys than HOCM. Caspase-3 and Ang II might play a role in renal tubular cell apoptosis induced by contrast media. Telmisartan protected the renal tissue from nephrotoxicity induced by contrast media.
PURPOSE: To evaluate the nephrotoxicity of high- and low-osmolar contrast media (HOCM, LOCM) on kidneys in Sprague-Dawley rats. Telmisartan was administered to confirm its protective role against nephrotoxicity induced by contrast media.
MATERIAL AND METHODS: Sixty male rats were randomly divided into six groups (n=10/group). Glycerin was given to all rats except controls to induce renal injury. HOCM (diatrizoate) or LOCM (iohexol) (10 ml/kg b.w., 300 mg I/ml) was given through a caudal vein. Serum creatinine level was measured by an automatical biochemical analyzer. Caspase-3 activity and Angiotensin II (Ang II) level of renal tissue were detected by fluorometric method and radioimmunoassay, respectively. The renal injury was also assessed by hematoxylin and eosin and TdT-mediated deoxyuridine nick end-labeling staining.
RESULTS: In diatrizoate-injected rats, serum creatinine level was increased (P<0.001). There was no significant difference between iohexol animals and glycerol controls in the level of serum creatinine. The renal caspase-3 activity and Ang II levels in HOCM and LOCM groups were higher than those in glycerol control group (P<0.001). The percentage of apoptotic tubular cells and pathological scores were lower in the iohexol animals than that in the diatrizoate animals (P<0.001). In the groups pretreated with telmisartan, no increase in the levels of serum creatinine, renal Ang II, and caspase-3 activity was observed (P>0.05). The renal injuries induced by contrast media were alleviated.
CONCLUSION: Both HOCM (diatrizoate) and LOCM (iohexol) could cause renal tubular cell apoptosis in the kidneys damaged by glycerin. LOCM was less toxic to rat kidneys than HOCM. Caspase-3 and Ang II might play a role in renal tubular cell apoptosis induced by contrast media. Telmisartan protected the renal tissue from nephrotoxicity induced by contrast media.