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沙棘原花青素是氧化应激下巨噬细胞线粒体功能的保护剂。

Sea Buckthorn Proanthocyanidins are the Protective Agent of Mitochondrial Function in Macrophages Under Oxidative Stress.

作者信息

Liu Keshan, Li Wenxia, Yuen Michael, Yuen Tina, Yuen Hywel, Wang Min, Peng Qiang

机构信息

College of Food Science and Engineering, Northwest A&F University, Yangling, China.

Puredia Limited, Xining, China.

出版信息

Front Pharmacol. 2022 Jul 8;13:914146. doi: 10.3389/fphar.2022.914146. eCollection 2022.

DOI:10.3389/fphar.2022.914146
PMID:35873561
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9307083/
Abstract

Sea buckthorn proanthocyanidins (SBP) are the most important antioxidant components of sea buckthorn, which are widely used in functional foods and cosmetics. Studies have shown that SBP have significant protective effects on macrophages against oxidative stress induced by hydrogen peroxide (HO). However, the mechanism remains uncertain. In the present study, we explored the effects of SBP on mitochondrial function and the mechanism of their protective effects against oxidative stress in cells. Our results showed that SBP could increase mitochondrial membrane potential, inhibit mPTP opening, reduce mitochondrial swelling, and enhance mitochondrial synthesis and metabolism. Thus, they alleviated oxidative damage and protected the cells against mitochondrial function. Western blot analysis showed that SBP had a protective effect on RAW264.7 cells by activating the AMPK-PGC1α-Nrf2 pathway. These results showed that SBP alleviated mitochondrial damage and dysfunction caused by oxidative stress. This study revealed the mechanism of SBP in reducing oxidative damage and provided a theoretical basis for further research on natural bioactive compounds to exert antioxidant activity and prevent arteriosclerosis and other diseases.

摘要

沙棘原花青素(SBP)是沙棘最重要的抗氧化成分,广泛应用于功能性食品和化妆品中。研究表明,SBP对巨噬细胞抵抗过氧化氢(HO)诱导的氧化应激具有显著的保护作用。然而,其机制仍不确定。在本研究中,我们探讨了SBP对线粒体功能的影响及其对细胞氧化应激的保护作用机制。我们的结果表明,SBP可以增加线粒体膜电位,抑制线粒体通透性转换孔(mPTP)开放,减少线粒体肿胀,并增强线粒体合成与代谢。因此,它们减轻了氧化损伤并保护细胞免受线粒体功能损害。蛋白质印迹分析表明,SBP通过激活AMPK-PGC1α-Nrf2途径对RAW264.7细胞具有保护作用。这些结果表明,SBP减轻了氧化应激引起的线粒体损伤和功能障碍。本研究揭示了SBP减少氧化损伤的机制,并为进一步研究天然生物活性化合物发挥抗氧化活性及预防动脉硬化等疾病提供了理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0853/9307083/8b300d345f75/fphar-13-914146-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0853/9307083/be4b8441d5f2/fphar-13-914146-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0853/9307083/08d188157fc0/fphar-13-914146-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0853/9307083/859a8ca16c66/fphar-13-914146-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0853/9307083/8b300d345f75/fphar-13-914146-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0853/9307083/be4b8441d5f2/fphar-13-914146-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0853/9307083/08d188157fc0/fphar-13-914146-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0853/9307083/859a8ca16c66/fphar-13-914146-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0853/9307083/8b300d345f75/fphar-13-914146-g004.jpg

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