摘要
目的探讨饱和氢盐水对电离辐射诱发的脑组织损伤的保护作用。方法成年4月龄健康SD大鼠45只,采用随机数字表法分为健康对照组,盐水治疗组和氢水治疗组,再根据照射后时间分为1、3、7和14d4个时间组,每组5只。4MeV电子线对大鼠进行单次垂直全脑照射,吸收剂量率为200cGy/min,吸收剂量20Gy。氢水治疗组大鼠于照射后即刻、照后连续3d给予饱和氢盐水腹腔注射,分别于照射后1、3、7和14d处死大鼠,取脑组织制作匀浆,分光光度计检测超氧化物歧化酶(SOD)、丙二醛(MDA)、8-羟基脱氧鸟嘌呤(8-OHdG)含量。HE染色观察海马区脑组织病理变化。结果7和14d时氢水治疗组脑组织含水量明显小于盐水治疗组(t=3.78、3.18,P〈0.05),SOD水平1—7d时氢水治疗组明显高于盐水治疗组(t=2.41—2.92,P〈0.05),MDA水平明显低于盐水治疗组(t=4.01—6.03,P〈0.05),持续到14d,8-OHdG含量1—7d氢水治疗组明显低于盐水治疗组(t=2.33、2.71、2.33,P〈0.05)。海马区神经细胞损伤明显轻于对照组。结论饱和氢盐水对大鼠急性放射性脑损伤早期有保护作用。
Objective To investigate the effect of hydrogen on radiation-induced acute injury in rat brain. Methods Forty-five mature Sprague-Dawley rats were randomly divided into three groups: saline therapy group, hydrogen therapy group and healthy control group. The whole brain of SD rat was irradiated with single dose of 20 Gy by 4 MeV electrons. Rats in therapy group were injected with hydrogen-rich saline after irradiation and were sacrificed at 1, 3, 7, 14 d post-irradiation. The changes of malonaldehyde (MDA), superoxidase dismutase (SOD) and 8-hydroxydeoxygunosine (8-OHdG) in brain homogenate and the pathological changes in brain hippocampus were observed. Results The brain water content ( t = 3.78,3.18 ,P 〈 0.05 ) and the contents of 8-OHdG ( t = 2. 33, 2.71, 2. 33 ,P 〈 0.05 ) in the therapy group was lower than the control group at 7 d and 14 d post-irradiation. The contents of SOD were significantly higher(t = 2.41 - 2. 92, P 〈 0. 05 ) from 1 to 7 day, while the contents of MDA were significantly lower in therapy group than those in the control group from 1 to 14 day post-irradiation ( t = 4.01- 6. 20, P 〈 0.05). Moreover, the damage degree in the nerve cells of hippocampus was less compared to the control group. Conclusions The hydrogen-rich saline could have protection role in irradiation-induced acute brain injury in rats.
出处
《中华放射医学与防护杂志》
CAS
CSCD
北大核心
2012年第5期485-487,共3页
Chinese Journal of Radiological Medicine and Protection
基金
基金项目:江苏省十二五医学重点学科(实验室)资助
关键词
氢气
辐射
防护
脑损伤
自由基
Hydrogen
Irradiation
Protection
Brain injury
Free radical