s -Ethyl cysteine, an amino acid derivative, attenuated cisplatin induced nephrotoxicity
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ORIGINAL ARTICLE
s‑Ethyl cysteine, an amino acid derivative, attenuated cisplatin induced nephrotoxicity Huey‑Liang Kuo1 · Mei‑Chin Mong2 · Hung‑Chih Chen3 · Zhi‑Hong Wang2 · Mei‑Chin Yin2,4 Received: 27 April 2020 / Accepted: 10 August 2020 © Springer-Verlag GmbH Austria, part of Springer Nature 2020
Abstract Renal protection from s-ethyl cysteine (SEC) against cisplatin (CP)-induced inflammatory and oxidative injury was examined. Mice were divided into five groups: normal group, 0.25% SEC group, CP group, 0.125% SEC + CP group, 0.25% SEC + CP group. After 2 weeks supplementation, mice of CP and SEC + CP groups received CP treatment. H&E stain showed that CP caused infiltration of inflammatory cells and necrosis of tubular cells. SEC pre-treatments attenuated CP-induced inflammatory injury and degeneration. SEC pre-treatments limited CP-stimulated release of interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha and prostaglandin E2 in kidney. CP raised the renal activity and mRNA expression of cyclooxygenase-2 and nuclear factor kappa B. SEC pre-treatments reversed these alterations. CP increased the production of reactive oxygen species and nitric oxide, and lowered glutathione content, glutathione peroxidase and glutathione reductase activities in kidney. SEC pre-treatments reversed these changes. CP up-regulated renal inducible nitric oxide synthase (iNOS) mRNA expression, and down-regulated nuclear factor E2-related factor (Nrf)-2 and heme oxygenase (HO)-1 mRNA expression. SEC pre-treatments suppressed iNOS mRNA expression; and enhanced renal Nrf2 and HO-1 mRNA expression. These novel findings suggest that dietary SEC via exerting its multiple bio-functions could be considered as a protective agent for kidney against CP. Keywords Cisplatin · s-Ethyl cysteine · Nephrotoxicity · Nrf2 · HO-1 Abbreviations AKI Acute kidney injury ALT Alanine transaminase ARE Antioxidant-response element AST Aspartate transaminase BUN Blood urea nitrogen BW Body weight Handling Editor: G. J. Peters. Huey-Liang Kuo and Mei-Chin Mong equally contributed to this study. * Mei‑Chin Yin [email protected] 1
Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan
2
Department of Food Nutrition and Health Biotechnology, Asia University, Taichung, Taiwan
3
Division of Nephrology, Asia University Hospital, Taichung, Taiwan
4
Department of Medical Research, China Medical University Hospital, Taichung, Taiwan
COX Cyclooxygenase CP Cisplatin Cr Creatinine DCFH-DA Dichlorofluorescein diacetate FI Feed intake GFR Glomerular filtration rate GPX Glutathione peroxidase GR Glutathione reductase GSH Glutathione HO Heme oxygenase IL Interleukin iNOS Inducible nitric oxide synthase NF-κB Nuclear factor kappa B NO Nitric oxide Nrf2 Nuclear factor E2-related factor 2 PGE Prostaglandin E ROS Reactive oxygen species RT-PCR Real-time polymerase chain reaction SEC s-Ethyl cysteine TNF Tumor necrosis factor WI Water intake
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Introduction Cisplatin (CP)
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