Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan.
Department of Food Nutrition and Health Biotechnology, Asia University, Taichung, Taiwan.
Amino Acids. 2020 Aug;52(8):1181-1190. doi: 10.1007/s00726-020-02882-9. Epub 2020 Aug 13.
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 E 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.
本研究旨在探讨 S-乙基半胱氨酸（SEC）对顺铂（CP）诱导的炎症和氧化损伤的肾脏保护作用。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。在 2 周补充后，CP 和 SEC+CP 组的小鼠接受 CP 处理。H&E 染色显示 CP 引起炎症细胞浸润和肾小管细胞坏死。SEC 预处理减轻 CP 诱导的炎症损伤和变性。SEC 预处理限制 CP 刺激的肾脏白细胞介素（IL）-1β、IL-6、肿瘤坏死因子-α和前列腺素 E 的释放。CP 增加肾环氧化酶-2 和核因子 kappa B 的活性和 mRNA 表达。SEC 预处理逆转了这些改变。CP 增加活性氧和一氧化氮的产生，降低肾脏谷胱甘肽含量、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 iNOS mRNA 表达；并增强肾 Nrf2 和 HO-1 mRNA 表达。这些新发现表明，膳食 SEC 通过发挥其多种生物功能，可被视为一种保护肾脏免受 CP 损伤的药物。
