Curcumin protects mitochondria from oxidative damage and attenuates apoptosis in cortical neurons

Yuan-gui ZHU; Xiao-chun CHEN; Zhi-zhe CHEN; Yu-qi ZENG; Guang-bin SHI; Yan-hua SU; Xu PENG

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Curcumin protects mitochondria from oxidative damage and attenuates apoptosis in cortical neurons

机译：姜黄素可保护线粒体免受氧化损伤并减弱皮层神经元的凋亡

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AIM: To investigate the effect of curcumin on tert-butyl hydroperoxide (t-BHP)-induced oxidative damage in rat cortical neurons and to explore the possible mechanism. METHODS: Primary cultured rat cortical neurons were performed in vitro and cell viability was measured by MTT assay. DNA fragmentation was used to evaluate cell apoptosis. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (△ψm) was determined by flow cytometric assay. Cellular glutathione (GSH) content was measured by spectrophotometer. Bcl-2family proteins, cytochrome c, cleaved caspase-3, and poly (ADP-ribose) polymerase (PARP) were detected by Western blot. RESULTS: Exposure of tBHP 100μmol/L to neurons for 60 min resulted in Aψm loss and cytochrome c release from mitochondria and subsequent activation of caspase-3 and PARP cleavation, and cell apoptosis.After removal of tBHP and then further treatment with curcumin (2.5-20μmol/L) for 18 h, curcumin abrogated △ψm loss and cytochrome c release, blocked activation of caspase 3, and altered the expression of Bcl-2 family.Further curcumin treatment also prevented cellular GSH and decreased intracellular ROS generation markedly.Curcumin eventually attenuated tBHP-induced apoptosis in cortical neurons. CONCLUSION: Curcumin may attenuate oxidative damages in cortical neurons by reducing intracellular production of ROS and protecting mitochondria from oxidative damage.

机译：目的：研究姜黄素对叔丁基过氧化氢（t-BHP）诱导的大鼠皮层神经元氧化损伤的影响，并探讨其可能的机制。方法：体外培养原代培养的大鼠皮质神经元，MTT法测定细胞活力。 DNA片段化用于评估细胞凋亡。通过流式细胞术测定细胞内活性氧（ROS）和线粒体膜电位（△ψm）。用分光光度计测量细胞内谷胱甘肽（GSH）的含量。通过蛋白质印迹法检测Bcl-2家族蛋白，细胞色素c，裂解的caspase-3和聚（ADP-核糖）聚合酶（PARP）。结果：将100μmol/ L的tBHP暴露于神经元60分钟导致线粒体Aψm丢失和细胞色素c释放，随后caspase-3活化和PARP裂解以及细胞凋亡。去除tBHP后再用姜黄素进一步治疗（2.5 -20μmol/ L）处理18 h，姜黄素消除了△ψm的丧失和细胞色素c的释放，阻断了caspase 3的活化，并改变了Bcl-2家族的表达;进一步的姜黄素处理还阻止了细胞GSH的产生并显着降低了细胞内ROS的产生。最终减弱了tBHP诱导的皮质神经元凋亡。结论：姜黄素可能通过减少细胞内ROS的产生并保护线粒体免受氧化损伤而减轻皮层神经元的氧化损伤。

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来源
《中国药理学报：英文版》 |2004年第12期|1606-1612|共7页
作者
Yuan-gui ZHU; Xiao-chun CHEN; Zhi-zhe CHEN; Yu-qi ZENG; Guang-bin SHI; Yan-hua SU; Xu PENG;
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作者单位

Rush University Medical Center, Chicago, IL 60612,USA;

Fujian Institute of Hematology,Fujian Medical University, Fuzhou 350001, China;

Union Hospital,Fujian Medical University, Fuzhou 350001, China;

Fujian Institute of Geriatrics,Fujian Medical University, Fuzhou 350001, China;

Fujian Institute of Geriatrics,Fujian Medical University, Fuzhou 350001, China;

Fujian Institute of Geriatrics,Fujian Medical University, Fuzhou 350001, China;

Fujian Institute of Geriatrics,Fujian Medical University, Fuzhou 350001, China;

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正文语种 chi
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Curcumin; tert-butyl hydroperoxide; apoptosis; oxidative stress; Bcl-2 family proteins; mitochondria; Alzheimer disease;

机译：姜黄素;氢过氧化叔丁基;细胞凋亡;氧化应激;Bcl-2家族蛋白;线粒体;阿尔茨海默病;

Curcumin protects mitochondria from oxidative damage and attenuates apoptosis in cortical neurons

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