目的:利用秀丽线虫研发合适的低氧损伤模型,以更好地揭示低氧生理和低氧病理的分子机制。方法:通过对秀丽线虫进行不同时间的低氧处理,系统观察线虫的死亡率、运动功能、细胞形态及相关蛋白表达水平的变化,分析低氧对线虫的损伤情况。结果:氧浓度为0.2%的物理性低氧可引起秀丽线虫多种细胞形态发生变化,进而导致线虫死亡,且死亡率随低氧时间延长而持续增加,同时低氧诱导因子(HIF-1)的表达显著上调。进一步通过神经元特异性转基因(绿色荧光蛋白)株系观察到低氧可引起神经元特征性损伤。结论:成功建立有效、简便易行的线虫物理低氧损伤模型,可用于低氧病理和低氧应答分子机制研究。
Objective: To develop a suitable hypoxic injury model, which is important for revealing pathological molecular mechanism of hypoxia. Methods: We focused on C. elegans by treatment with different hypoxie times and systematically observed mortality, movement, cellular morphology and the related-pretein expression of the animals. Results: We demonstrated that hypoxia (0.2% partial pressure of oxygen) induced morphological cell defects, and then leading to death of C. elegans. The mortality of C. elegans increased along with hypoxie time, while hypoxia-inducible factor(HIF-1) was significantly up-regulated. In addition, by using neuron-specific transgeuic worms with green fluorescent protein- we observed the neuron-specific injury caused by hypoxic stress. Conclusion: We successfully established an effective, convenient physical hypoxic model of C. elegans, which will facilitate the studies of hypoxic pathology and molecular mechanisms of hypoxic response in the future.