L-carnitine suppresses cisplatin-induced renal injury in rats: impact on cytoskeleton proteins expression

Osama Fouad Ahmed Ebrahim; Ola Elsayed Nafea; Walaa Samy; Lamiaa Mohamed Shawky

doi:10.1093/toxres/tfaa092

L-carnitine suppresses cisplatin-induced renal injury in rats: impact on cytoskeleton proteins expression

Toxicol Res (Camb). 2021 Jan 5;10(1):51-59. doi: 10.1093/toxres/tfaa092. eCollection 2021 Jan.

Authors

Osama Fouad Ahmed Ebrahim¹, Ola Elsayed Nafea², Walaa Samy³, Lamiaa Mohamed Shawky⁴

Affiliations

¹ Department of Anatomy, Faculty of Medicine, Benha University, Benha 13518, Egypt.
² Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Zagazig University, Zagazig 44519, Egypt.
³ Department of Medical Biochemistry, Faculty of Medicine, Zagazig University, Zagazig 44519, Egypt.
⁴ Department of Histology and Cell Biology, Faculty of Medicine, Benha University, Benha 13518, Egypt.

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.

Keywords: L-carnitine; cisplatin; gap junction proteins; intermediate filaments; podocyte.