Chang Yung-Ting, Huang Chiung-Yao, Tang Jen-Yang, Liaw Chih-Chuang, Li Ruei-Nian, Liu Jing-Ru, Sheu Jyh-Horng, Chang Hsueh-Wei
Doctoral Degree Program in Marine Biotechnology, National Sun Yat-sen University, Kaohsiung, Taiwan.
Doctoral Degree Program in Marine Biotechnology, Academia Sinica, Taipei, Taiwan.
Onco Targets Ther. 2017 Jul 4;10:3289-3297. doi: 10.2147/OTT.S138123. eCollection 2017.
We previously reported that the soft coral-derived bioactive substance, sinuleptolide, can inhibit the proliferation of oral cancer cells in association with oxidative stress. The functional role of oxidative stress in the cell-killing effect of sinuleptolide on oral cancer cells was not investigated as yet. To address this question, we introduced the reactive oxygen species (ROS) scavenger (-acetylcysteine [NAC]) in a pretreatment to evaluate the sinuleptolide-induced changes to cell viability, morphology, intracellular ROS, mitochondrial superoxide, apoptosis, and DNA damage of oral cancer cells (Ca9-22). After sinuleptolide treatment, antiproliferation, apoptosis-like morphology, ROS/mitochondrial superoxide generation, annexin V-based apoptosis, and γH2AX-based DNA damage were induced. All these changes were blocked by NAC pretreatment at 4 mM for 1 h. This showed that the cell-killing mechanism of oral cancer cells of sinuleptolide is ROS dependent.
我们之前报道过,源自软珊瑚的生物活性物质——柳珊瑚内酯,可通过氧化应激抑制口腔癌细胞的增殖。然而,氧化应激在柳珊瑚内酯对口腔癌细胞的细胞杀伤作用中的功能作用尚未得到研究。为了解决这个问题,我们在预处理中引入了活性氧(ROS)清除剂N-乙酰半胱氨酸(NAC),以评估柳珊瑚内酯诱导的口腔癌细胞(Ca9-22)的细胞活力、形态、细胞内ROS、线粒体超氧化物、凋亡和DNA损伤的变化。柳珊瑚内酯处理后,诱导了细胞增殖抑制、凋亡样形态、ROS/线粒体超氧化物生成、基于膜联蛋白V的凋亡以及基于γH2AX的DNA损伤。在4 mM NAC预处理1小时后,所有这些变化均被阻断。这表明柳珊瑚内酯对口腔癌细胞的细胞杀伤机制是ROS依赖性的。
Pharmaceuticals (Basel). 2021-9-29
Environ Toxicol. 2017-9
Environ Toxicol. 2017-11-22
Antioxidants (Basel). 2021-10-10
J Pers Med. 2021-8-31
Antioxidants (Basel). 2021-9-2
Antioxidants (Basel). 2021-7-13
Antioxidants (Basel). 2021-6-30
Antioxidants (Basel). 2020-11-13