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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Collagen Type III, Creatinine, Fibrosis, Kidney, Lithotripsy, Male, Models, Animal, NF-kappa B, Proline, Rats, Rats, Sprague-Dawley, Signal Transduction, Thiocarbamates, Transforming Growth Factor beta1.
user
Does shock wave induce chronic renal lesion through activation of the nuclear factor kappa B signaling pathway? Context: 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. 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. 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.
assistant
NFκB plays an important role in the progression of shock-wave- induced long-term renal damage in rat model. Final Decision: yes