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.

研究了肾脏对s-乙基半胱氨酸（SEC）的抵抗顺铂（CP）引起的炎症和氧化损伤的保护作用。将小鼠分为五组：正常组，0.25％SEC组，CP组，0.125％SEC + CP组，0.25％SEC + CP组。补充2周后，CP和SEC + CP组的小鼠接受CP治疗。H＆E染色显示CP引起炎症细胞浸润和肾小管细胞坏死。SEC预处理可减轻CP引起的炎症损伤和变性。SEC预处理可限制CP刺激的白介素（IL）-1beta，IL-6，肿瘤坏死因子-α和前列腺素E ₂的释放在肾脏。CP增强了肾脏的活动和环氧合酶2和核因子κB的mRNA表达。SEC预处理逆转了这些改变。CP增加了肾脏中活性氧和一氧化氮的产生，并降低了谷胱甘肽含量，谷胱甘肽过氧化物酶和谷胱甘肽还原酶活性。SEC预处理逆转了这些变化。CP上调肾诱导型一氧化氮合酶（iNOS）mRNA表达，下调核因子E2相关因子（Nrf）-2和血红素加氧酶（HO）-1 mRNA表达。SEC预处理抑制了iNOS mRNA的表达。并增强肾脏Nrf2和HO-1 mRNA表达。这些新颖的发现表明，饮食SEC通过发挥其多种生物功能可以被认为是肾脏对抗CP的保护剂。