Abstract
Aristolochic acid (AA) nephropathy exhibits early proximal tubular injury and fatty acid metabolic disorder. In order to study the unrecognized abnormalities of organic ion transporters and fatty acid metabolism indicators in AA nephropathy, Wistar rats were orally administrated with vehicle, 10 and 20 mg/kg AA once daily for 7 days, respectively. At day 8, significant reduction of body weight and right kidney weight, as well as elevation of plasma blood urea nitrogen (BUN) levels, renal long-chain fatty acids (LCFAs), non-esterified fatty acids (NEFA) and triglycerides (TG) contents were observed in AA-treated rats, accompanying with down-regulation of renal rOAT1/3, rOCT1/2 and rOCTN1/2 expressions. OCTN2 particularly transports l-carnitine through cell membrane. AA treatment also induced a significant decrease of l-carnitine levels in renal cortex of rats. Down-regulation of peroxisome proliferator-activated receptor alpha (rPPARα) and carnitine acyltransferase 1 (rCPT1), and up-regulation of acetyl coenzyme A carboxylase 1/2 (rACC1/2) in renal cortex were detected in AA-treated rats. These results indicate that alterations of organic ion transportation and fatty acid metabolism are part of AA-induced nephropathy (AAN), contribute to the altered urinary metabolic profile and may lead to further proximal tubule injury in rats.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
