Staff Members - Benha University
l-Carnitine Suppresses Cisplatin-Induced Renal Injury in Rats: Impact on Cytoskeleton Proteins Expression
Toxicology Research • 2021
Publication Information
Authors
Osama Fouad Ahmed Ebrahim,1 Ola Elsayed Nafea, 2,3,∗ Walaa Samy4
and Lamiaa Mohamed Shawky5
Keywords
Not Available
Journal
Toxicology Research
Publisher
Not Available
Volume
10
Issue
Not Available
Pages
51–59
publication.type
Local
Paper Link
Not Available
Supplementary Materials
Not Available
Abstract
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
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