对氧化应激的Nrf2依赖性适应可以防止糖尿病病症的进展
Eugene Lee1, Jae-Hun Ahn2, Byeong-Cheol Kang2
1Renal Pathology Lab, Hankook Kidney and Diabetes Research Center, Seoul, Korea.
Antioxidants & redox signaling
|November 12, 2024
概括
棕酸 (PA) 和omega-3脂肪酸EPA/DHA影响细胞中氧化应激适应. EPA/DHA激活Nrf2-免疫蛋白酶体通路,防止糖尿病病的进展.
科学领域:
- 细胞生物学 细胞生物学
- 分子机制的分子机制
- 代谢障碍 代谢障碍 代谢障碍
背景情况:
- 氧化应激适应对于细胞平衡至关重要.
- 棕酸 (PA) 和omega-3脂肪酸 (EPA/DHA) 在糖尿病中影响氧化应激和免疫蛋白酶调节.
- Nrf2在细胞和糖尿病脏中调解这些效应的作用尚未完全理解.
研究的目的:
- 在与糖尿病病 (DN) 相关的模型中,研究Nrf2在PA和EPA/DHA诱导的氧化应激下Nrf2/免疫蛋白酶体通路中的Nrf2的作用.
主要方法:
- 宝细胞对PA,EPA和DHA的短期和长期暴露.
- 对Nrf2活性,抗氧化蛋白表达和免疫蛋白酶水平的分析.
- 在体内研究使用db/db小鼠食富含EPA/DHA鱼油.
主要成果:
- 短时间的PA暴露上调了Nrf2和免疫蛋白酶体,赋予了急性氧化应激适应.
- 通过Nrf2激活,EPA/DHA诱导了持续的氧化应激适应.
- 长时间暴露于PA降低了Nrf2活性,这种效应被EPA/DHA减弱.
- 富含EPA/DHA的鱼油通过增加脏Nrf2和免疫蛋白酶体,抑制了db/db小鼠的DN进展.
结论:
- 和EPA/DHA不同调节受Nrf2介导的氧化应激适应在细胞和脏.
- EPA/DHA激活Nrf2-免疫蛋白酶体通路,减轻糖尿病病中蛋白质毒性压力.
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