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三氧化二砷诱导大鼠神经胶质瘤细胞凋亡及活性氧的形成。

Arsenic trioxide induces apoptosis and the formation of reactive oxygen species in rat glioma cells.

机构信息

1Nursing Support Center, First Affiliated Hospital, Harbin Medical University, Harbin, 150000 China.

2Neurosurgery Department, First Affiliated Hospital, Harbin Medical University, Nangang District, Harbin, 150000 China.

出版信息

Cell Mol Biol Lett. 2018 Mar 27;23:13. doi: 10.1186/s11658-018-0074-4. eCollection 2018.

DOI:10.1186/s11658-018-0074-4
PMID:29610575
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5870496/
Abstract

BACKGROUND

Arsenic trioxide (AsO) has a dramatic therapeutic effect on acute promyelocytic leukemia (APL) patients. It can also cause apoptosis in various tumor cells. This study investigated whether AsO has an antitumor effect on glioma and explored the underlying mechanism.

RESULTS

MTT and trypan blue assays showed that AsO remarkably inhibited growth of C6 and 9 L glioma cells. Cell viability decreased in glioma cells to a greater extent than in normal glia cells. The annexin V-FITC/PI and Hoechest/PI staining assays revealed a significant increase in apoptosis that correlated with the duration of AsO treatment and occurred in glioma cells to a greater extent than in normal glial cells. AsO treatment induced reactive oxygen species (ROS) production in C6 and 9 L cells in a time-dependent manner. Cells pretreated with the antioxidant N-acetylcysteine (NAC) showed significantly lower AsO-induced ROS generation. AsO significantly inhibited the expression of the anti-apoptotic gene Bcl-2, and upregulated the proapoptotic gene Bax in both C6 and 9 L glioma cells in a time-dependent manner.

CONCLUSIONS

AsO can significantly inhibit the growth of glioma cells and it can induce cell apoptosis in a time- and concentration-dependent manner. ROS were found to be responsible for apoptosis in glioma cells induced by AsO. These results suggest AsO is a promising agent for the treatment of glioma.

摘要

背景

三氧化二砷（AsO）对急性早幼粒细胞白血病（APL）患者具有显著的治疗作用。它还可以诱导多种肿瘤细胞凋亡。本研究探讨了三氧化二砷（AsO）对神经胶质瘤是否具有抗肿瘤作用，并探讨了其潜在的机制。

结果

MTT 和台盼蓝检测结果显示，AsO 可显著抑制 C6 和 9L 神经胶质瘤细胞的生长。与正常神经胶质细胞相比，神经胶质瘤细胞的活力下降更为明显。 Annexin V-FITC/PI 和 Hoechest/PI 染色检测显示，细胞凋亡显著增加，且与 AsO 处理时间呈正相关，神经胶质瘤细胞的凋亡程度大于正常神经胶质细胞。AsO 处理可在时间依赖性方式下诱导 C6 和 9L 细胞中活性氧（ROS）的产生。抗氧化剂 N-乙酰半胱氨酸（NAC）预处理的细胞中，AsO 诱导的 ROS 生成明显降低。AsO 可显著抑制 C6 和 9L 神经胶质瘤细胞中抗凋亡基因 Bcl-2 的表达，并呈时间依赖性地上调促凋亡基因 Bax。

结论

AsO 可显著抑制神经胶质瘤细胞的生长，并呈时间和浓度依赖性诱导细胞凋亡。ROS 是 AsO 诱导神经胶质瘤细胞凋亡的原因。这些结果表明 AsO 是治疗神经胶质瘤的一种有前途的药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c12/5870496/c185cf755766/11658_2018_74_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c12/5870496/9f3a780ec5a2/11658_2018_74_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c12/5870496/520811b52c58/11658_2018_74_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c12/5870496/00a6b159452a/11658_2018_74_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c12/5870496/9d492fea5f71/11658_2018_74_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c12/5870496/c185cf755766/11658_2018_74_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c12/5870496/9f3a780ec5a2/11658_2018_74_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c12/5870496/520811b52c58/11658_2018_74_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c12/5870496/00a6b159452a/11658_2018_74_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c12/5870496/9d492fea5f71/11658_2018_74_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c12/5870496/c185cf755766/11658_2018_74_Fig5_HTML.jpg

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