Diabetic nephropathy (DN) is the major life-threatening complication of diabetes, and oxidative stress takes part in its initiation and development. This study was performed to evaluate the effects of carotenoids from Sporidiobolus pararoseus (CSP) on the renal function and oxidative stress status of mice with streptozotocin (STZ)-induced DN. The results indicated that CSP significantly attenuated symptoms of STZ-induced DN shown by decreased fasting blood glucose, reduced urine volume, urine albumin, serum creatinine and serum urea nitrogen, and improved kidney histological morphology. Furthermore, biochemical analysis of serum and kidney revealed a marked increase in oxidative stress of DN mice as evidenced by reduced total antioxidant capacity (T-AOC), decreased activity of antioxidant enzyme -superoxide dismutase (SOD) and increased level of malondialdehyde (MDA). However, treatment with CSP improved oxidative stress status in DN mice as compared with the mice in model group. Exploration of the potential mechanism validated that CSP ameliorated the oxidative stress status in DN mice by activating the expressions of Nrf2, NQO-1, HO-1, GST and CAT in kidney. These data revealed that CSP may retard the progression of DN by ameliorating renal function, improving the oxidative stress status and activating the Nrf2/ARE pathway.

中文翻译：

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Sporidiobolus pararoseus中的类胡萝卜素通过减轻氧化应激改善小鼠糖尿病肾病

糖尿病肾病 (DN) 是糖尿病的主要危及生命的并发症，氧化应激参与了其发生和发展。本研究旨在评估来自 Sporidiobolus pararoseus (CSP) 的类胡萝卜素对链脲佐菌素 (STZ) 诱导的 DN 小鼠肾功能和氧化应激状态的影响。结果表明，CSP 可显着减轻 STZ 诱导的 DN 症状，表现为空腹血糖降低、尿量减少、尿白蛋白、血清肌酐和血清尿素氮减少，并改善肾脏组织学形态。此外，血清和肾脏的生化分析显示 DN 小鼠的氧化应激显着增加，这可以通过总抗氧化能力 (T-AOC) 降低来证明，抗氧化酶-超氧化物歧化酶 (SOD) 活性降低，丙二醛 (MDA) 水平升高。然而，与模型组小鼠相比，CSP 治疗改善了 DN 小鼠的氧化应激状态。潜在机制的探索证实了CSP通过激活肾脏中Nrf2、NQO-1、HO-1、GST和CAT的表达来改善DN小鼠的氧化应激状态。这些数据表明，CSP 可能通过改善肾功能、改善氧化应激状态和激活 Nrf2/ARE 通路来延缓 DN 的进展。潜在机制的探索证实了CSP通过激活肾脏中Nrf2、NQO-1、HO-1、GST和CAT的表达来改善DN小鼠的氧化应激状态。这些数据表明，CSP 可能通过改善肾功能、改善氧化应激状态和激活 Nrf2/ARE 通路来延缓 DN 的进展。潜在机制的探索证实了CSP通过激活肾脏中Nrf2、NQO-1、HO-1、GST和CAT的表达来改善DN小鼠的氧化应激状态。这些数据表明，CSP 可能通过改善肾功能、改善氧化应激状态和激活 Nrf2/ARE 通路来延缓 DN 的进展。