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作 者:李红霞[1] 崔谊[1] 徐延杰[1] 李福艳[1] 史文琦[1] 王建震 曾庆师[1]
出 处:《中华放射肿瘤学杂志》2017年第2期228-233,共6页Chinese Journal of Radiation Oncology
基 金:国家自然科学基金(81372439)
摘 要:目的应用高分辨率MR氢谱检测大鼠脑胶质瘤细胞系C6的放射损伤并初步探讨其机制。方法以C6细胞为研究对象,应用MR氢谱检测细胞内多种代谢物浓度;彗星实验检测DNA损伤;流式细胞术检测周期进程及凋亡率;克隆形成实验观察克隆形成率并初步探讨放射损伤作用机制。采用单因素方差分析,Pearson法相关分析。结果照射剂量由0Gy增加为1、5、10、15Gy时,DNA损伤逐渐加重且有剂量依赖性(P=0.000~0.690),G1期所占百分比显著增加(P=0.026—0.749),凋亡率逐渐上升(P=0.000~0.000),克隆形成率逐渐降低(P=0.000—0.004);同时,代谢物比值Lac/Cr逐渐减少(P=0.000-0.015),与DNA损伤参数(尾长、彗尾中DNA含量、尾矩)呈线性负相关(r=-0.971、-0.998、-0.995),与凋亡率呈线性负相关(r=-0.978)。结论MR氢谱检测发现C6细胞照射后Lac/Cr比值变化与肿瘤细胞凋亡有明显相关性,MR氢谱具有预测脑胶质瘤放射损伤的潜力。Objective To study the radiation injury of rat C6 glioma cell line by high resolution, ^1H-nuclear magnetic resonance (^1H NMR ) spectroscopy, and to preliminarily investigate its mechanism. Methods Metaholite concentrations in C6 cells were determined by ^1H NMR spectroscopy. Comet assay was used to evaluate DNA damage. Flow eytometry was used to determine the cell cycle and apoptosis rate. Colony-forming assay was used to measure the colony-forming rate and preliminarily investigate the mechanism of radiation injury. The results were analyzed by one-way analysis of variance and Pearson correlation analysis. Results With the increase in radiation dose from 0 Gy to 1, 5, 10, and 15 Gy, DNA damage was enhanced in a dose-dependent manner (P= 0. 000-0. 690) ;the percentage of cells in G1 phase increased (P = 0. 026-0. 749) ;the apoptosis rate significantly increased ( all P = 0. 000) ;the colony-forming rate significantly declined ( P = 0. 000-0. 004) ;the Lae/Cr ratio significantly decreased ( P = 0. 000-0. 015 ), which had a negative linear correlation with DNA damage parameters (tail length, r=-0. 971 ;%DNA in the tail, r = - 0. 998 ; tail moment, r = - 0. 995 ) and apoptosis rate ( r = 0. 978 ). Conclusions t H NMR spectroscopy reveals that the change in the Lac/Cr ratio is associated with injury and apoptosis of C6 cells after radiation. ^1H NMR spectroscopy has the potential to predict radiation injury of glioma.
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