Shen Yin, Zhao Hong-Yang, Wang Hai-Jun, Wang Wen-Liang, Zhang Li-Zhi, Fu Rong
Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
J Huazhong Univ Sci Technolog Med Sci. 2016 Aug;36(4):554-557. doi: 10.1007/s11596-016-1624-5. Epub 2016 Jul 28.
The expression changes of Rars gene in ischemia-injured neurons were investigated by detecting its translational product arginyl-tRNA synthetase (ArgRS), and the inhibitory effects of ischemic preconditioning (IPC) on Rars gene were explored. Both IPC model and prolonged ischemia (PI) model were established by using the classic oxygen glucose deprivation (OGD) method. The primary cultured neurons were assigned into the following groups: the experimental group (IPC+PI group), undergoing PI after a short period of IPC; the conditional control group (PI control group), subjected to PI without IPC; blank control group, the normally cultured neurons. The Rars transcriptional activities and ArgRS expression levels were measured at different time points after re-oxygenation (3 h/6 h/12 h/24 h). Data were collected and statistically analyzed. Compared to the blank control group, the Rars activities and ArgRS levels were significantly increased in PI control group, peaking at the time point of 6 h after re-oxygenation. Rars activities and ArgRS levels were significantly lower in the experimental group than in the PI control group at different time points after re-oxygenation. PI insult can induce an escalating activity of Rars and lead to ArgRS over-expression in primary cultured neurons. IPC can inhibit the increased Rars activity and down-regulate ArgRS expression of ischemia-insulted neurons. This mechanism may confer ischemic tolerance on neurons.
通过检测Rars基因的翻译产物精氨酰 - tRNA合成酶（ArgRS），研究其在缺血损伤神经元中的表达变化，并探讨缺血预处理（IPC）对Rars基因的抑制作用。采用经典的氧糖剥夺（OGD）方法建立IPC模型和长时间缺血（PI）模型。将原代培养的神经元分为以下几组：实验组（IPC + PI组），在短时间IPC后进行PI；条件对照组（PI对照组），接受PI但未进行IPC；空白对照组，正常培养的神经元。在复氧后不同时间点（3小时/6小时/12小时/24小时）测量Rars转录活性和ArgRS表达水平。收集数据并进行统计学分析。与空白对照组相比，PI对照组的Rars活性和ArgRS水平显著升高，在复氧后6小时达到峰值。复氧后不同时间点，实验组的Rars活性和ArgRS水平均显著低于PI对照组。PI损伤可诱导原代培养神经元中Rars活性升高并导致ArgRS过表达。IPC可抑制缺血损伤神经元中Rars活性的增加并下调ArgRS表达。这一机制可能赋予神经元缺血耐受性。
