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黄芩提取物和类黄酮可保护 L6 细胞免受安密霉素 A 诱导的线粒体功能障碍。

Scutellaria baicalensis Extracts and Flavonoids Protect Rat L6 Cells from Antimycin A-Induced Mitochondrial Dysfunction.

机构信息

Korea Institute of Oriental Medicine, 461-24 Jeonmin-dong, Yuseong-gu, Daejeon 305-811, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2012;2012:517965. doi: 10.1155/2012/517965. Epub 2012 Aug 30.

Abstract

Antimycin A (AMA) damages mitochondria by inhibiting mitochondrial electron transport and can produce reactive oxygen species (ROS). ROS formation, aging, and reduction of mitochondrial biogenesis contribute to mitochondrial dysfunction. The present study sought to investigate extracts of Scutellaria baicalensis and its flavonoids (baicalin, baicalein, and wogonin), whether they could protect mitochondria against oxidative damage. The viability of L6 cells treated with AMA increased in the presence of flavonoids and extracts of S. baicalensis. ATP production decreased in the AMA treated group, but increased by 50% in cells treated with flavonoids (except wogonin) and extracts of S. baicalensis compared to AMA-treated group. AMA treatment caused a significant reduction (depolarized) in mitochondrial membrane potential (MMP), whereas flavonoid treatment induced a significant increase in MMP. Mitochondrial superoxide levels increased in AMA treated cells, whereas its levels decreased when cells were treated with flavonoids or extracts of S. baicalensis. L6 cells treated with flavonoids and extracts of S. baicalensis increased their levels of protein expression compared with AMA-treated cells, especially water extracts performed the highest levels of protein expression. These results suggest that the S. baicalensis extracts and flavonoids protect against AMA-induced mitochondrial dysfunction by increasing ATP production, upregulating MMP, and enhancing mitochondrial function.

摘要

安密霉素 A(AMA)通过抑制线粒体电子传递损害线粒体,并能产生活性氧(ROS)。ROS 的形成、衰老和线粒体生物发生的减少导致线粒体功能障碍。本研究旨在探讨黄芩提取物及其黄酮类化合物(黄芩苷、黄芩素和汉黄芩素)是否能保护线粒体免受氧化损伤。存在黄酮类化合物和黄芩提取物时,用 AMA 处理的 L6 细胞的存活率增加。与 AMA 处理组相比,AMA 处理组的 ATP 产量下降,但用黄酮类化合物(除汉黄芩素外)和黄芩提取物处理的细胞的 ATP 产量增加了 50%。AMA 处理导致线粒体膜电位(MMP)显著降低(去极化),而黄酮类化合物处理诱导 MMP 显著增加。在 AMA 处理的细胞中,线粒体超氧水平增加,而在用黄酮类化合物或黄芩提取物处理的细胞中,其水平降低。与 AMA 处理的细胞相比,用黄酮类化合物和黄芩提取物处理的 L6 细胞增加了其蛋白表达水平,尤其是水提取物表现出最高的蛋白表达水平。这些结果表明,黄芩提取物和黄酮类化合物通过增加 ATP 产生、上调 MMP 和增强线粒体功能来防止 AMA 诱导的线粒体功能障碍。

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