Key Laboratory of Developmental Genes and Human Diseases in Ministry of Education, Medical School, Southeast University, Nanjing, 210009, China.
College of Biology and Food Engineering, Chongqing Three Gorges University, Wanzhou, 404100, China.
Ecotoxicol Environ Saf. 2019 Nov 15;183:109554. doi: 10.1016/j.ecoenv.2019.109554. Epub 2019 Aug 18.
Due to short life cycle, nematode Caenorhabditis elegans is a suitable animal model for assessing the effect of long-term simulated microgravity treatment on organisms. We here investigated the effect of simulated microgravity treatment for 24-h on development and functional state of intestinal barrier in nematodes. Simulated microgravity treatment not only caused a broadened intestinal lumen, but also enhanced intestinal permeability. Intestinal overexpression of SOD-2, a mitochondrial Mn-SOD protein, prevented the damage on functional state of intestinal barrier by simulated microgravity and induced a resistance to toxicity of simulated microgravity, suggesting the crucial role of oxidative stress in inducing the damage on functional state of intestinal barrier in simulated microgravity treated nematodes. For the molecular basis of damage on functional state of intestinal barrier, we observed significant decrease in expressions of some genes (acs-22, erm-1, and hmp-2) required for maintenance of functional state of intestinal barrier in simulated microgravity treated nematodes. Our results highlight the potential of long-term simulated microgravity treatment in inducing intestinal damage in animals.
由于生命周期短,秀丽隐杆线虫是评估长期模拟微重力处理对生物体影响的合适动物模型。在这里,我们研究了模拟微重力处理 24 小时对线虫肠道屏障发育和功能状态的影响。模拟微重力处理不仅导致肠道腔变宽,还增强了肠道通透性。肠道中超表达 Mn-SOD 蛋白 SOD-2 可防止模拟微重力对肠道屏障功能状态的损害,并诱导对模拟微重力毒性的抗性,表明氧化应激在诱导模拟微重力处理的线虫肠道屏障功能状态损害中起关键作用。对于肠道屏障功能状态损害的分子基础,我们观察到在模拟微重力处理的线虫中,一些维持肠道屏障功能状态所需的基因(acs-22、erm-1 和 hmp-2)的表达显著下降。我们的结果强调了长期模拟微重力处理在诱导动物肠道损伤方面的潜力。