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从芍药中分离得到的芍药苷能减轻抗霉素 A 诱导的成骨细胞毒性。

Paeoniflorin isolated from Paeonia lactiflora attenuates osteoblast cytotoxicity induced by antimycin A.

机构信息

Department of Food & Nutrition, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea.

出版信息

Food Funct. 2013 Sep;4(9):1332-8. doi: 10.1039/c3fo60147a.

Abstract

The protective effects of paeoniflorin isolated from Paeonia lactiflora against pharmacological inhibition of the respiratory chain were studied using osteoblastic MC3T3-E1 cells. Here we show that paeoniflorin decreases cell death induced by antimycin A, an inhibitor of mitochondrial complex III. Paeoniflorin restored antimycin A-induced inactivation of phosphoinositide 3-kinase (PI3K) and thioredoxin reductase, suggesting that PI3K and thioredoxin reductase may be involved in paeoniflorin-induced cytoprotective responses. We also examined the effect of paeoniflorin on mitochondrial dysfunction and oxidative stress induced by antimycin A. Paeoniflorin inhibited mitochondrial membrane potential dissipation, ATP loss, inactivation of complexes I and IV, cytochrome c release, and cardiolipin oxidation induced by antimycin A. In addition, paeoniflorin prevented antimycin A-induced ROS release and nitrotyrosine increase. These results imply that paeoniflorin protects osteoblasts from antimycin A-induced cell death via improved mitochondrial function.

摘要

芍药苷(从芍药中分离得到的化合物)对呼吸链的药理学抑制具有保护作用,本研究采用成骨细胞 MC3T3-E1 细胞对此进行了研究。结果表明,芍药苷可降低抗霉素 A(一种线粒体复合物 III 抑制剂)诱导的细胞死亡。芍药苷恢复了抗霉素 A 诱导的磷酸肌醇 3-激酶(PI3K)和硫氧还蛋白还原酶失活,提示 PI3K 和硫氧还蛋白还原酶可能参与芍药苷诱导的细胞保护反应。我们还研究了芍药苷对抗霉素 A 诱导的线粒体功能障碍和氧化应激的影响。芍药苷抑制了抗霉素 A 诱导的线粒体膜电位耗散、ATP 丢失、复合物 I 和 IV 失活、细胞色素 c 释放和心磷脂氧化。此外,芍药苷还可防止抗霉素 A 诱导的 ROS 释放和硝基酪氨酸增加。这些结果表明,芍药苷通过改善线粒体功能保护成骨细胞免受抗霉素 A 诱导的细胞死亡。

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