Abstract
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.
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