[秀丽隐杆线虫物理缺氧模型的建立与应用]
[Development and application of the physical hypoxic models of C. elegans].
作者信息
Ren Chang-hong, Zhang Ji-ye, Shi Jin-ping, Jiang Bin, Zhao Na, Liu Hu-qi, Zhang Cheng-gang
机构信息
Beijing Institute of Radiation Medicine, State Key Laboratory of Proteomics, State Key Laboratory of Medical Neurobiology, Beijing 100850, China.
出版信息
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2011 Aug;27(3):257-62.
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 hypoxic times and systematically observed mortality, movement, Cellular morphology and the related-protein 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 hypoxic time, while hypoxia-inducible factor (HIF-1) was significantly up-regulated. In addition, by using neuron-specific transgenic wonns with green fluorescent protein--we observed the neuron-specffic 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.
目的
建立一种合适的缺氧损伤模型，这对于揭示缺氧的病理分子机制具有重要意义。
方法
我们通过不同缺氧时间处理秀丽隐杆线虫，并系统观察动物的死亡率、运动情况、细胞形态以及相关蛋白表达。
结果
我们证明缺氧（氧分压0.2%）诱导细胞形态缺陷，进而导致秀丽隐杆线虫死亡。秀丽隐杆线虫的死亡率随缺氧时间增加，而缺氧诱导因子（HIF-1）显著上调。此外，通过使用带有绿色荧光蛋白的神经元特异性转基因线虫，我们观察到缺氧应激引起的神经元特异性损伤。
结论
我们成功建立了一种有效、便捷的秀丽隐杆线虫物理缺氧模型，这将有助于未来对缺氧病理学和缺氧反应分子机制的研究。
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