Journal
TOXICOLOGY RESEARCH
Volume 10, Issue 1, Pages 51-59Publisher
OXFORD UNIV PRESS
DOI: 10.1093/toxres/tfaa092
Keywords
cisplatin; gap junction proteins; intermediate filaments; L-carnitine; podocyte
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LCAR has shown a curative effect on CDDP-induced kidney injury in rats by reversing renal structural and functional impairments, lowering serum urea and creatinine concentrations, restoring oxidant/antioxidant balance, reversing inflammation, and inhibiting caspase 3-mediated apoptotic cell death in renal tissues. Additionally, LCAR effectively down-regulates cytoskeleton proteins mRNA levels, reflecting amelioration of CDDP-induced podocyte injury.
We designed this work to examine the curative role of L-carnitine (LCAR) in a rat model of cisplatin (CDDP)-induced kidney injury. We induced kidney injury in rats by a single intraperitoneal injection of 5 mg/kg of CDDP. Fifteen days post injection, rats were orally supplemented with 354 mg/kg of LCAR for another 15 days. Kidney tissues were subjected to histo-biochemical analysis along with mRNA gene expression quantification for cytoskeleton proteins encoding genes (vimentin, nestin, and connexin 43) by real-time reverse transcription polymerase chain reaction. LCAR reversed CDDP-induced renal structural and functional impairments. LCAR significantly declined serum urea and creatinine concentrations, restored oxidant/antioxidant balance, reversed inflammation, and antagonized caspase 3-mediated apoptotic cell death in renal tissues. Moreover, LCAR effectively down-regulated cytoskeleton proteins mRNA levels, reflecting amelioration of CDDP-provoked podocyte injury. We concluded that LCAR has a favorable therapeutic utility against CDDP-induced kidney injury.
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