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目的探讨硫酸镁对电离辐射诱发的脑组织损伤的保护作用。方法将成熟的SD大鼠36只随机分为空白对照组、实验对照组和硫酸镁实验用药组,用6 MeV电子线对实验组大鼠进行20 Gy全脑单次垂直照射,吸收剂量率为200 cGy/min,分别于照射后1、3、7和14 d解剖大鼠行腹主动脉取血,取其脑组织,用酶联免疫吸附法(ELISA)测定血清神经元特异性稀醇化酶(NSE)含量,Western blot方法检测大鼠脑组织N-甲基-D-天门冬氨酸受体NR1及NR2B蛋白表达量的变化。结果与空白对照组相比,实验对照组大鼠血清NSE含量及脑组织NR1和NR2B蛋白表达量升高,各时间点血清NSE含量差异均有统计学意义(P<0.05);实验用药组与实验对照组相比,照射后1d血清NSE含量差异没有统计学意义(P>0.05),但随着照射后观察时间的延长,NSE含量出现显著降低,差异有统计学意义(P<0.05),直到14d仍然未恢复至正常水平;实验用药组大鼠脑组织NR1和NR2B蛋白表达量在照射后的各时间点与实验对照组相比,均有所降低。结论早期使用硫酸镁可降低照射后血清NSE的含量及脑组织NR1和NR2B蛋白表达量,硫酸镁对急性放射性脑损伤有保护作用。
Objective To investigate the protective effect of magnesium sulfate on the damage of brain tissue induced by ionizing radiation. Methods Thirty-six adult Sprague-Dawley rats were randomly divided into blank control group, experimental control group and magnesium sulfate experimental group. The single dose of 20 Gy whole brain was irradiated by 6 MeV electron beam, and the dose rate was 200 cGy / min. The rats were sacrificed at 1, 3, 7 and 14 days after irradiation to take the blood of abdomen aorta. The brain tissues were taken out and the levels of serum neuron specific isoenzyme (NSE) were detected by immunohistochemistry. The expression of N-methyl-D-aspartate receptor NR1 and NR2B protein in rat brain were detected by Western blot. Results Compared with the blank control group, the serum NSE level and the expression of NR1 and NR2B protein in the experimental group were significantly increased (P <0.05). The experimental group and Compared with the control group, there was no significant difference in serum NSE level at 1 day after irradiation (P> 0.05). However, the NSE level decreased significantly with the prolonged observation time after irradiation (P <0.05) The level of NR1 and NR2B protein in brain tissue of rats in experimental group decreased at all time points after irradiation compared with the control group. Conclusion Early use of magnesium sulfate can reduce the level of serum NSE and the expression of NR1 and NR2B protein in brain tissue. Magnesium sulfate has a protective effect on acute radiation-induced brain injury.