College of Food Science and Technology, Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Guangdong Provincial Science and Technology Innovation Center for Subtropical Fruit and Vegetable Processing, Zhanjiang 524088, China.
School of Food Science and Engineering, South China University of Technology, Guangzhou 510641, China.
Food Funct. 2022 Aug 1;13(15):8204-8213. doi: 10.1039/d2fo00474g.
Mitochondrial function is closely related to the body's oxidative stress level and lifespan. Our previous research demonstrated that the combination of blueberry extracts (BE) and apple peel extracts (APE) could synergistically promote the oxidative stress and lifespan of (). The purpose of this study was to determine whether the improvement of the oxidative stress and lifespan is involved in the regulation of mitochondrial function, and to explore its potential mechanisms. A model of nematode mitochondrial dysfunction was established using RNAi technology. The results showed that supplementation with BE plus APE could prolong the lifespan of RNAi() , and improve mitochondrial function, while there was no significant effect on RNAi() . In addition, treatment with BE plus APE could down-regulate the overexpression of reactive oxygen species (ROS) in () mutants. Meanwhile, administration with BE plus APE abolished the extension of the lifespan of () mutants, and inhibited the expression of downstream genes, including , , , , and , thereby regulating the function of the mitochondrial respiratory chain and improving its oxidative stress ability to prolong the lifespan of nematodes. In short, the combination of BE and APE could improve the oxidative stress and extend the lifespan of nematodes regulating mitochondrial function. This study provided a theoretical basis for exploring the role of mitochondrial function in regulating the body's oxidative stress level and aging process.
线粒体功能与机体氧化应激水平和寿命密切相关。本课题组前期研究表明，蓝莓提取物（BE）和苹果皮提取物（APE）联合使用具有协同促进氧化应激和寿命的作用。本研究旨在探讨这种协同作用是否通过调节线粒体功能来实现，并进一步探索其潜在机制。采用 RNAi 技术构建线虫线粒体功能障碍模型。结果表明，BE+APE 联合补充可延长 RNAi()线虫的寿命，并改善线粒体功能，但对 RNAi()线虫无明显影响。此外，BE+APE 处理可下调()突变体中线粒体中活性氧（ROS）的过度表达。同时，BE+APE 的给药消除了()突变体寿命的延长，并抑制了下游基因如 、 、 、 、 和 的表达，从而调节线粒体呼吸链的功能，提高其氧化应激能力，延长线虫的寿命。总之，BE 和 APE 的联合使用可以通过调节线粒体功能来改善线虫的氧化应激和延长寿命。本研究为探索线粒体功能在调节机体氧化应激水平和衰老过程中的作用提供了理论依据。
