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纸质出版:2012
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张礼均,胡荣,李飞,孟辉,林江凯,朱刚,王宪荣,冯华.去铁胺对大鼠大脑冲击伤的治疗作用[J].陆军军医大学学报(原第三军医大学学报),2012,34(23):2349-2352.
Zhang Lijun,Hu Rong,Li Fei,Meng Hui,Lin Jiangkai,Zhu Gang,Wang Xianrong,Feng Hua.Deferoxamine attenuates traumatic brain injury in rats[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(23):2349-2352.
张礼均,胡荣,李飞,孟辉,林江凯,朱刚,王宪荣,冯华.去铁胺对大鼠大脑冲击伤的治疗作用[J].陆军军医大学学报(原第三军医大学学报),2012,34(23):2349-2352. DOI:
Zhang Lijun,Hu Rong,Li Fei,Meng Hui,Lin Jiangkai,Zhu Gang,Wang Xianrong,Feng Hua.Deferoxamine attenuates traumatic brain injury in rats[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(23):2349-2352. DOI:
目的 探讨去铁胺对大鼠大脑冲击伤的治疗作用。 方法 健康成年雄性SD大鼠39只,分为假手术组、致伤组和去铁胺(deferoxamine
DFO)治疗组,每组13只。参照Feeney法致伤,假手术组只开颅,不打击,致伤组和DFO治疗组开颅后,打击部位和打击量完全一致,致伤后2 h分别予以等量生理盐水及去铁胺100 mg/kg腹腔注射,间隔12 h给药,持续28 d,并于1、3、7、14、28 d检测大鼠血红蛋白、肛温、血糖和死亡率,于处死前进行Morris水迷宫实验,处死后取大鼠大脑标本运用多田公式计算大鼠大脑缺损体积,并取致伤灶周围脑组织进行NeuN免疫荧光检测。 结果 各组大鼠同一时相点血红蛋白、肛温、血糖差异均无统计学差异(P0.05),致伤灶和DFO治疗组病死率差异无统计学意义(P0.05)。DFO治疗组大脑缺损体积(115.35±13.70)mm
3
较致伤组(209.99±16.70)mm
3
明显减小(P0.05)。免疫荧光检测发现致伤组致伤灶周围难以见到神经元,而DFO治疗组则可见到大量神经元。Morris水迷宫实验发现DFO治疗组动物平台搜索策略(3.13±0.35)和搜索时间(36.15±26.63)s均较致伤组[分别为(2.13±0.64)、(110.00±47.34)s
]
显著改善(P0.05)。 结论 大鼠大脑冲击伤后早期予以DFO治疗,能显著减轻大脑缺损体积和致伤灶周围神经元损伤,并改善大鼠空间学习记忆能力,提示DFO可能是改善颅脑创伤预后的有效药物。
Objective To determine the effect of deferoxamine (DFO) administration on traumatic brain injury (TBI) in rats. Methods A total of 39 male Sprague-Dawley rats were randomly and equally divided into 3 groups
sham-operation group
TBI group and DFO treatment group. Modified Feeney’s method was used to establish the rat model of experimental TBI with an impact of a weight of 30 g from 15 cm after craniotomy. The rats of DFO tr
eatment group were intraperitoneally injected with 100 mg/kg DFO in 2 h after TBI and then at 12-hour intervals for up to 28 d
and those of the other 2 groups were treated with same volume of normal saline. Rectal temperature
blood glucose and hemoglobin were detected at 1
3
7
14 and 28 d after injury
and the total mortality was recorded. After Morris water maze was performed to assess rat behavior
all rats were sacrificed. Then the volume of defected brain was detected with Coniglobus formula
and the expression of NeuN around the injury site was detected with immunofluorescence staining. Results There was no significant difference in rectal temperature
blood glucose
hemoglobin
and mortality at the different time points among different groups (P0.05). The volume of defected brain after TBI was smaller in rats of DFO-treated group than in injury group (115.35±13.70 vs 209.99±16.70 mm
3
P0.05). Immunofluorescence staining indicated that there was no NeuN positive cell in the TBI group
while many NeuN positive cells were found in DFO treatment group. The strategy of research platform (3.13±0.35) and the time of research platform (36.15±26.63 s) in DFO treatment group were greatly ameliorated than those in TBI group (2.13±0.64 and 110.00±47.34 s
P0.05). Conclusion Early administration of DFO significantly attenuates pathological damage in rats after TBI
and improves the ability of space learning and memory
which suggest that DFO may be an effective drug in treatment of acute TBI.
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