首页> 外文期刊>International Journal of Radiation Biology: Covering the Physical, Chemical, Biological, and Medical Effects of Ionizing and Non-ionizing Radiations >Emodin, an anthraquinone derivative, protects against gamma radiation-induced toxicity by inhibiting DNA damage and oxidative stress
【24h】

Emodin, an anthraquinone derivative, protects against gamma radiation-induced toxicity by inhibiting DNA damage and oxidative stress

机译:大黄素,一种蒽醌衍生物,可通过抑制DNA损伤和氧化应激来防止伽玛射线引起的毒性

获取原文
获取原文并翻译 | 示例
           

摘要

Purpose: In the present study, we explored the modulatory effect of emodin (1,3,8-trihydroxy-6-methylanthraquinone, C15H10O 5) against gamma radiation-induced DNA damage and oxidative stress in acellular and cellular systems, respectively. Materials and methods: For cellular systems, concanavalin A (ConA)-stimulated murine splenocytes were used. Cytotoxic effect of emodin (0-400 μM), radiation (3-12 Gy) and emodin + radiation was measured by MTT [3-(4,5-dimethylthiazol-2-yl) 2,5- diphenyltetrazolium bromide] assay. Gamma radiation (3-12 Gy)-induced production of reactive oxygen species (ROS), an increase in nitric oxide (NO) level and its inhibition by emodin were estimated by DCFDA (2′,7′- dichlorofluorescein diacetate) and Griess regent, respectively. Analysis of radiation-induced apoptosis was performed using flow cytometery and acridine orange/ethidium bromide staining. DNA damage was evaluated in acellular system using pBR322 plasmid relaxation assay. Results: Emodin was able to effectively scavenge radiation-induced free radicals (ROS and NO) in murine splenocytes. Radiation-induced apoptosis and cell death was also inhibited by emodin pre-treatment. It could significantly prevent radiation-induced DNA damage. Conclusions: Protection against gamma radiation-induced cell death and DNA damage by emodin could be attributed to its free radical scavenging activity. The present study is the first report of the radioprotective role of emodin in mammalian cells.
机译:目的:在本研究中,我们探讨了大黄素(1,3,8-三羟基-6-甲基蒽醌,C15H10O 5)对γ-射线诱导的脱细胞和细胞系统DNA损伤和氧化应激的调节作用。材料和方法:对于细胞系统,使用伴刀豆球蛋白A(ConA)刺激的鼠脾细胞。大黄素(0-400μM),放射线(3-12 Gy)和大黄素+放射线的细胞毒性作用通过MTT [3-(4,5-二甲基噻唑-2-基)2,5-二苯基四唑溴化物]测定来测量。 DCFDA(2',7'- dichlorofluorescein diacetate)和Griess regent估计了伽马射线(3-12 Gy)诱导的活性氧(ROS)的产生,一氧化氮(NO)水平的增加及其对大黄素的抑制作用, 分别。使用流式细胞仪和a啶橙/溴化乙锭染色对放射线诱导的细胞凋亡进行分析。使用pBR322质粒松弛试验在脱细胞系统中评估DNA损伤。结果:大黄素能够有效清除小鼠脾细胞中辐射诱导的自由基(ROS和NO)。大黄素预处理还可以抑制辐射诱导的细胞凋亡和细胞死亡。它可以显着防止辐射引起的DNA损伤。结论:大黄素对γ射线诱导的细胞死亡和DNA损伤的保护作用可能归因于其清除自由基的活性。本研究是大黄素在哺乳动物细胞中的辐射防护作用的首次报道。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号