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阿朴啡因对阿霉素 A 诱导的成骨细胞 MC3T3-E1 细胞损伤的保护作用。

Protective effect of apocynin on antimycin A-induced cell damage in osteoblastic MC3T3-E1 cells.

机构信息

Department of Food and Nutrition, Education Graduate School, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, Korea.

出版信息

J Appl Toxicol. 2012 Sep;32(9):714-21. doi: 10.1002/jat.1689. Epub 2011 May 2.

Abstract

Apocynin is a naturally occurring methoxy-substituted catechol, experimentally used as an inhibitor of NADPH-oxidase. In the present study, we investigated the protective effects of apocynin on antimycin A (AMA)-induced toxicicy in osteoblastic MC3T3-E1 cells. Exposure of MC3T3-E1 cells to AMA caused significant cell viability loss, as well as mitochondrial membrane potential (MMP) dissipation, complex IV inactivation, ATP loss, intracellular calcium ([Ca2+]i) elevation and oxidative stress. Pretreatment with apocynin prior to AMA exposure significantly reduced AMA-induced cell damage by preventing MMP dissipation, complex IV inactivation, ATP loss, [Ca2+]i elevation and oxidative stress. These results suggest that apocynin has a protective effect against AMA-induced cell damage by its antioxidant effects and the attenuation of mitochondrial dysfunction. Apocynin also induced the activation of PI3K (phosphoinositide 3-kinase), Akt (protein kinase B) and CREB (cAMP-response element-binding protein) inhibited by AMA. All these data indicate that apocynin may reduce or prevent osteoblasts degeneration in osteoporosis or other degenerative disorders.

摘要

阿朴肉桂酸是一种天然存在的甲氧基取代儿茶酚,实验中用作 NADPH 氧化酶抑制剂。在本研究中,我们研究了阿朴肉桂酸对抗霉素 A(AMA)诱导的成骨细胞 MC3T3-E1 细胞毒性的保护作用。暴露于 AMA 的 MC3T3-E1 细胞导致细胞活力显著丧失,以及线粒体膜电位(MMP)耗散、复合物 IV 失活、ATP 损失、细胞内钙([Ca2+]i)升高和氧化应激。在暴露于 AMA 之前用阿朴肉桂酸预处理可通过防止 MMP 耗散、复合物 IV 失活、ATP 损失、[Ca2+]i 升高和氧化应激来显著减轻 AMA 诱导的细胞损伤。这些结果表明,阿朴肉桂酸通过其抗氧化作用和减轻线粒体功能障碍对 AMA 诱导的细胞损伤具有保护作用。阿朴肉桂酸还诱导了 AMA 抑制的 PI3K(磷酸肌醇 3-激酶)、Akt(蛋白激酶 B)和 CREB(cAMP 反应元件结合蛋白)的激活。所有这些数据表明,阿朴肉桂酸可能减少或预防骨质疏松症或其他退行性疾病中的成骨细胞退化。

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