title: Shock wave induces chronic renal lesion through activation of the nuclear factor kappa B signaling pathway.
abstract: OBJECTIVE
  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.
  
  
  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.
  
  
  CONCLUSIONS
  NFκB plays an important role in the progression of shock-wave- induced long-term renal damage in rat model.
authors.affiliation: Department of Urology, First Affiliated hospital, Medical College, Xi'an Jiaotong University, Xi'an, No.277 Yanta West Road, Xi'an, Shaanxi Province 710061, China.
authors.forename: Xiang
authors.initials: X
authors.lastname: Li
authors.forename: Yuquan
authors.initials: Y
authors.lastname: Xue
authors.forename: Dalin
authors.initials: D
authors.lastname: He
authors.forename: Xingfa
authors.initials: X
authors.lastname: Chen
authors.forename: Linlin
authors.initials: L
authors.lastname: Zhang
mesh_terms: D000818:Animals; D024061:Collagen Type III / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D005355:Fibrosis; D007668:Kidney / Q000293:injuries / Q000378:metabolism* / Q000473:pathology*; D008096:Lithotripsy / Q000009:adverse effects*; D008297:Male; D023421:Models, Animal; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011392:Proline / Q000031:analogs & derivatives / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000502:physiology*; D013859:Thiocarbamates / Q000494:pharmacology; D053773:Transforming Growth Factor beta1 / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D024061:Collagen Type III; D016328:NF-kappa B; D013859:Thiocarbamates; D053773:Transforming Growth Factor beta1; C066229:prolinedithiocarbamate; D011392:Proline; D003404:Creatinine