Shock wave induces chronic renal lesion through activation of the nuclear factor kappa B signaling pathway

• Published in: World journal of urology Vol. 28; no. 5; pp. 657 - 662
• Main Authors: Li, Xiang, Xue, Yuquan, He, Dalin, Chen, Xingfa, Zhang, Linlin
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer-Verlag 01-10-2010; Springer; Springer Nature B.V
• Subjects: Animals; Biological and medical sciences; Collagen Type III - metabolism; Creatinine - blood; Fibrosis; Kidney - injuries; Kidney - metabolism; Kidney - pathology; Kidneys; Lithotripsy - adverse effects; Male; Medical sciences; Medicine; Medicine & Public Health; Models, Animal; Nephrology; Nephrology. Urinary tract diseases; NF-kappa B - antagonists & inhibitors; NF-kappa B - metabolism; Oncology; Original Article; Proline - analogs & derivatives; Proline - pharmacology; Rats; Rats, Sprague-Dawley; Signal Transduction - physiology; Thiocarbamates - pharmacology; Transforming Growth Factor beta1 - antagonists & inhibitors; Transforming Growth Factor beta1 - metabolism; Urinary system involvement in other diseases. Miscellaneous; Urology; Renal fibrosis; Inflammation; Extracorporeal shock wave lithotripsy; Kidney disease; Nephrology; Urinary system disease; Instrumentation therapy; Activation; Shock wave; Kidney; Urology; Chronic; Urinary system; Signaling pathway; Lithotripsy; Transcription factor NFκB; Lesion
• ISSN: 0724-4983; 1433-8726
• DOI: 10.1007/s00345-010-0515-9

Purpose
The mechanisms responsible for the pathogenesis of long-term renal damage induced by extracorporeal shock wave lithotripsy (ESWL) are not clear. The present study was designed to investigate the role of nuclear factor κB (NFκB) signal pathway in the pathogenesis of chronic shock wave-induced renal damage in rat model. Materials and methods: Adult male Sprague–Dawley rats were exposed to ESWL under the guidance of X-rays. On days 1, 3, 7, 35, and 105 postexposures to shock wave, the animals were killed to examine the changes in renal histology and functions, and NFκB activity. The expression of NFκB-dependent fibrogenic genes was also analyzed. Pyrrolidine dithiocarbamate (PDTC), a specific NFκB inhibitor, was used to further investigate the involvement of NFκB.
Results
The applied shock wave caused a transient decline in renal function and induced chronic morphological changes such as tubular injury and interstitial fibrosis. NFκB was significantly activated in renal cortex. PDTC had little or no effects on the shock-wave-induced transient renal damage, but attenuated the long-term renal lesions associated with NFκB activation. In addition, the shock wave exposure also up-regulated the expression of transforming growth factor-β1 (TGF-β1), which was also blocked by PDTC.
Conclusion
NFκB plays an important role in the progression of shock-wave- induced long-term renal damage in rat model.