Sonodynamic therapy induces oxidative stress, DNA damage and apoptosis in glioma cells

Sun Yue; Wang Haiping; Zhang Kun; Liu Jingfei; Wang Pan; Wang Xiaobing; Liu Quanhong

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Sonodynamic therapy induces oxidative stress, DNA damage and apoptosis in glioma cells

机译：SONOGYNAMIC THERAPACY在胶质瘤细胞中诱导氧化应激，DNA损伤和凋亡

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Malignant glioma remains one of the most challenging diseases to treat because of the invasive growth of glioma cells and the existence of the blood-brain barrier (BBB), which blocks drug delivery to the brain. New strategies are urgently needed to overcome these shortcomings and improve the outcomes. Ultrasound represents a promising noninvasive and reversible BBB opening approach and the related sonodynamic therapy (SDT) is rapidly emerging. This study aims to explore the ultrasound parameters for BBB opening and the cell killing effect of SDT in human glioma U373 cells by using a recently reported sonosensitizer, sinoporphyrin sodium (DVDMS). The in vitro BBB model indicated that SDT caused a time-dependent permeability increase, which peaked at 2 h post treatment and then recovered gradually. The results of toxicology tests showed significant U373 cell viability loss and apoptosis increase after DVDMS-SDT, accompanied by enhanced cleaved-caspase-3 level and DNA fragmentation, in which reactive oxygen species (ROS) were a major triggering intermediate during DVDMS-SDT. Furthermore, DVDMS-SDT produced DNA damage and the underlying mechanisms were evaluated, in order to provide a fundamental basis for DVDMS-SDT application in glioma therapy. The findings indicated that the DNA molecules could be temporarily regulated by SDT and DNA double-strand breaks (DSBs), which increased the difficulty of cellular self-repair, thus aggravating cell apoptosis and inhibiting glioma cell invasive growth. Therefore, this study supports the use of SDT as an alternative approach for glioma therapy.

机译：由于胶质瘤细胞的侵袭性生长和血脑屏障（BBB）的存在，恶性胶质瘤仍然是治疗最具挑战性的疾病之一，这阻止了药物递送给大脑的药物。迫切需要新的策略来克服这些缺点并改善结果。超声表示有前途的非侵入性和可逆的BBB开放方法，相关的铿son性治疗（SDT）正在迅速出现。本研究旨在通过使用最近报道的超声溶剂，中骨晶钠（DVDMS）探讨BBB开放和SDT在人胶质瘤U373细胞中SDT的细胞杀伤作用的超声参数。体外BBB模型表明，SDT导致时间依赖性渗透性增加，其在治疗后2小时达到达到峰值，然后逐渐回收。毒理学测试结果显示出明显的U373细胞活力损失和DVDMS-SDT后的凋亡增加，伴随着增强的切割 - caspase-3水平和DNA片段化，其中活性氧物质（ROS）在DVDMS-SDT期间是主要的触发中间体。此外，DVDMS-SDT产生的DNA损伤和基础机制得到评估，以便为胶质瘤治疗中的DVDMS-SDT应用提供基础。结果表明，DNA分子可以通过SDT和DNA双链（DSB）暂时调节，这增加了细胞自我修复的难度，从而加剧细胞凋亡并抑制胶质瘤细胞侵袭性生长。因此，本研究支持使用SDT作为胶质瘤治疗的替代方法。

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《RSC Advances》 |2018年第63期|共12页
作者
Sun Yue; Wang Haiping; Zhang Kun; Liu Jingfei; Wang Pan; Wang Xiaobing; Liu Quanhong;
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Shaanxi Normal Univ Natl Engn Lab Resource Dev Endangered Crude Drugs Key Lab Med Resources &

Nat Pharmaceut Chem Minist Educ Coll Life Sci Xian 710119 Shaanxi Peoples R China;

Shaanxi Normal Univ Natl Engn Lab Resource Dev Endangered Crude Drugs Key Lab Med Resources &

Nat Pharmaceut Chem Minist Educ Coll Life Sci Xian 710119 Shaanxi Peoples R China;

Shaanxi Normal Univ Natl Engn Lab Resource Dev Endangered Crude Drugs Key Lab Med Resources &

Nat Pharmaceut Chem Minist Educ Coll Life Sci Xian 710119 Shaanxi Peoples R China;

Shaanxi Normal Univ Natl Engn Lab Resource Dev Endangered Crude Drugs Key Lab Med Resources &

Nat Pharmaceut Chem Minist Educ Coll Life Sci Xian 710119 Shaanxi Peoples R China;

Shaanxi Normal Univ Natl Engn Lab Resource Dev Endangered Crude Drugs Key Lab Med Resources &

Nat Pharmaceut Chem Minist Educ Coll Life Sci Xian 710119 Shaanxi Peoples R China;

Shaanxi Normal Univ Natl Engn Lab Resource Dev Endangered Crude Drugs Key Lab Med Resources &

Nat Pharmaceut Chem Minist Educ Coll Life Sci Xian 710119 Shaanxi Peoples R China;

Shaanxi Normal Univ Natl Engn Lab Resource Dev Endangered Crude Drugs Key Lab Med Resources &

Nat Pharmaceut Chem Minist Educ Coll Life Sci Xian 710119 Shaanxi Peoples R China;

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1. LRIG1 cDNA诱导人胶质瘤细胞系H4凋亡的分子机制 [J] . 叶飞, 郭东升, 牛洪泉, 癌症（英文版） . 2004,第010期
2. Sonodynamic therapy induces oxidative stress, DNA damage and apoptosis in glioma cells [J] . Sun Yue, Wang Haiping, Zhang Kun, RSC Advances . 2018,第63期

机译：SONOGYNAMIC THERAPACY在胶质瘤细胞中诱导氧化应激，DNA损伤和凋亡
3. Enhancement of antitumor activity by using 5-ALA-mediated sonodynamic therapy to induce apoptosis in malignant gliomas: significance of high-intensity focused ultrasound on 5-ALA-SDT in a mouse glioma model [J] . Suehiro Satoshi, Ohnishi Takanori, Yamashita Daisuke, Journal of neurosurgery. . 2018,第6期

机译：通过使用5 alA介导的超声动力学治疗诱导恶性胶质瘤细胞凋亡的抗肿瘤活性的增强：高强度聚焦超声在小鼠胶质瘤模型中的5-Ala-SDT中的意义
4. Time course assessment of methylmercury effects on C6 glioma cells: submicromolar concentrations induce oxidative DNA damage and apoptosis. [J] . Belletti S, Orlandini G, Vettori MV, Journal of Neuroscience Research . 2002,第5期

机译：甲基汞对C6胶质瘤细胞的时程评估：亚微摩尔浓度可诱导DNA氧化损伤和细胞凋亡。
5. Iron Oxide Nanoparticles Induce Autophagy to inhibit Human Vascular Endothelial Cell Apoptosis caused by Oxidative Stress Damage [C] . Rongrong Jin, Jiuju Du, James M. Anderson, Society for Biomaterials annual meeting and exposition . 2017

机译：氧化铁纳米颗粒诱导自噬抑制氧化应激损伤引起的人类血管内皮细胞凋亡
6. Mechanism of 3,3'-diindolylmethane-induced cell death in human C33A cervical cancer cells: Induction of endoplasmic reticulum stress, apoptosis and the role of growth-arrest and DNA-damage genes [D] . Han, Jing Y. 2009

机译：3,3'-二吲哚基甲烷诱导的人C33A宫颈癌细胞死亡的机制：内质网应激，细胞凋亡以及生长停滞和DNA损伤基因的作用
7. Arsenic trioxide induces oxidative stress DNA damage and mitochondrial pathway of apoptosis in human leukemia (HL-60) cells [O] . Sanjay Kumar, Clement G Yedjou, Paul B Tchounwou 2014

机译：三氧化二砷诱导人白血病（HL-60）细胞氧化应激DNA损伤和线粒体凋亡途径
8. Correction: Sonodynamic therapy induces oxidative stress, DNA damage and apoptosis in glioma cells [O] . Yue Sun, Haiping Wang, Kun Zhang, 2021

机译：校正：SONOGYNAMIC THERICAPY在胶质瘤细胞中诱导氧化应激，DNA损伤和凋亡
9. 5-AED Enhances Survival of Irradiated Mice in a G-CSF-Dependent Manner, Stimulates Innate Immune Cell Function, Reduces Radiation-Induced DNA Damage and Induces Genes that Modulate Cell Cycle Progression and Apoptosis. [R] . Grace, M. B., Singh, V. K., Rhee, J. G., 2012

机译：5-aED以G-CsF依赖性方式增强辐照小鼠的存活，刺激先天免疫细胞功能，减少辐射诱导的DNa损伤并诱导调节细胞周期进展和细胞凋亡的基因。

Sonodynamic therapy induces oxidative stress, DNA damage and apoptosis in glioma cells

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