• DOI:10.1007/s00726-020-02882-9
• Corpus ID: 221123684

s-Ethyl cysteine, an amino acid derivative, attenuated cisplatin induced nephrotoxicity

@article{Kuo2020sEthylCA,
  title={s-Ethyl cysteine, an amino acid derivative, attenuated cisplatin induced nephrotoxicity},
  author={H L Kuo and Mei-chin Mong and Hung-Chih Chen and Zhi‐hong Wang and Mei-chin Yin},
  journal={Amino Acids},
  year={2020},
  volume={52},
  pages={1181 - 1190}
}

• H. Kuo, M. Mong, +2 authors M. Yin
• Published 1 August 2020
• Biology
• Amino Acids

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.