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丙戊酸钠可改善铝诱导的PC12细胞氧化应激和细胞凋亡。

Sodium valproate ameliorates aluminum-induced oxidative stress and apoptosis of PC12 cells.

作者信息

Iranpak Forough, Saberzadeh Jamileh, Vessal Mahmood, Takhshid Mohammad Ali

机构信息

Department of Biochemistry, Islamic Azad University of Shiraz, Shiraz, Iran.

Diagnostic Laboratory Sciences and Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

出版信息

Iran J Basic Med Sci. 2019 Nov;22(11):1353-1358. doi: 10.22038/ijbms.2019.36930.8804.

DOI:10.22038/ijbms.2019.36930.8804
PMID:32128102
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7038424/
Abstract

OBJECTIVES

According to recent studies, valproate shows some protection against oxidative stress (OS) induced by neurotoxins. Current investigation tried to determine the possible ameliorating effects of sodium valproate (SV) against aluminum (Al)-induced cell death, apoptosis, mitochondrial membrane potential (MMP), and OS in PC12 cells.

MATERIALS AND METHODS

In this in vitro study, PC12 cells were treated with different concentrations of aluminum maltolate (Almal) with and without SV (50-400 µM). Cell viability was assessed by MTT assay. To measure quantitatively the effects of SV on Al-induced apoptosis and reactive oxygen species (ROS), flowcytometry using 7AAD/annexin-V and 2', 7'-dichlorofluorescein diacetate staining were employed, respectively. MMP was monitored using the retention of rhodamine 123. Catalase (CAT) activity was assayed by the rate of decomposition of hydrogen peroxide.

RESULTS

Exposure of PC12 cells for 48 hr to Almal (125-2000 µM) significantly reduced cell viability (IC=1090 μM), increased ROS generation and apoptosis, and reduced MMP and CAT activity. SV reduced the Almal-induced cell death and apoptosis. Furthermore, the effects of Almal on ROS generation, catalase activity, and MMP reduction were significantly diminished by SV.

CONCLUSION

Data from this study suggest that SV can inhibit Al-induced cell death and apoptosis of PC12 cells via ameliorating OS.

摘要

目的

根据最近的研究,丙戊酸盐对神经毒素诱导的氧化应激(OS)具有一定的保护作用。当前的研究试图确定丙戊酸钠(SV)对铝(Al)诱导的PC12细胞死亡、凋亡、线粒体膜电位(MMP)和OS的可能改善作用。

材料与方法

在这项体外研究中,PC12细胞用不同浓度的苹果酸铝(Almal)处理,同时或不同时添加SV(50 - 400 μM)。通过MTT法评估细胞活力。为了定量测量SV对Al诱导的凋亡和活性氧(ROS)的影响,分别采用7AAD/膜联蛋白-V流式细胞术和2',7'-二氯荧光素二乙酸酯染色。使用罗丹明123的保留情况监测MMP。通过过氧化氢的分解速率测定过氧化氢酶(CAT)活性。

结果

PC12细胞暴露于Almal(125 - 2000 μM)48小时后,细胞活力显著降低(IC = 1090 μM),ROS生成和凋亡增加,MMP和CAT活性降低。SV减少了Almal诱导的细胞死亡和凋亡。此外,SV显著减轻了Almal对ROS生成、过氧化氢酶活性和MMP降低的影响。

结论

本研究数据表明,SV可通过改善OS抑制Al诱导的PC12细胞死亡和凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/bbc66527fee7/IJBMS-22-1353-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/faa3521fb6f9/IJBMS-22-1353-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/14ae24c99eef/IJBMS-22-1353-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/3cdfbfc2fee2/IJBMS-22-1353-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/84cf9fad4cf1/IJBMS-22-1353-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/19fcfb9d9e1c/IJBMS-22-1353-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/bbc66527fee7/IJBMS-22-1353-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/faa3521fb6f9/IJBMS-22-1353-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/14ae24c99eef/IJBMS-22-1353-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/3cdfbfc2fee2/IJBMS-22-1353-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/84cf9fad4cf1/IJBMS-22-1353-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/19fcfb9d9e1c/IJBMS-22-1353-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f186/7038424/bbc66527fee7/IJBMS-22-1353-g006.jpg

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