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目的研究照射前给予地西泮对放射性脑损伤大鼠血脑屏障的影响,探讨其对放射性脑损伤的防护作用机理。方法 240只SD大鼠随机分为4组,每组60只,D-R组:照射前30 min腹腔注射地西泮5 mg／kg;N-R组:照射前未用药;D-SR组:假照射(放置于照射野之外)前30 min腹腔注射地西泮5 mg／kg;N-SR组:假照射前未用药。D-R、N-R组建立清醒状态下大鼠放射性脑损伤模型。分别于照射前即刻、照射后6 h、1 d、1周和1月时记录磁共振成像(MRI)T1加权、T2加权的信号强度及其增强率,测定脑组织中伊文思蓝(EB)含量,免疫组化法分析海马神经元血管内皮生长因子(VEGF)的表达,并观察病理形态学的改变。结果 N-R组照射后T1加权的信号强度降低,T2加权的信号强度和信号强度的增强率升高,D-R组上述MRI的改变均比N-R组降低,D-R组脑组织EB含量在照射后6 h、1周和1月时及照射后6 h VEGF表达较N-R组降低(P<0．05或0．01)。结论在照射前使用地西泮通过降低脑组织VEGF表达,降低了放射性脑损伤大鼠血脑屏障的通透性,对放射性脑损伤有一定的防护作用。
Objective To study the effect of diazepam before irradiation on the blood-brain barrier in radiation-induced brain injury in rats and its protective mechanism on radiation-induced brain injury. Methods 240 Sprague-Dawley rats were randomly divided into 4 groups (n = 60 in each group): DR group: 5 mg / kg diazepam intraperitoneally 30 min before irradiation; NR group: no drug before irradiation; D-SR group: Placed in the radiation field outside) intraperitoneal injection of diazepam 5 mg / kg 30 min before; N-SR group: no irradiation before sham irradiation. D-R, N-R group, a rat model of radiation brain damage was established. The signal intensities and intensities of T1 weighted and T2 weighted magnetic resonance imaging (MRI) were recorded at 6 h, 1 d, 1 week and 1 month after irradiation, respectively. Evans blue (EB) The expression of vascular endothelial growth factor (VEGF) in hippocampal neurons was analyzed by immunohistochemistry and the pathomorphological changes were observed. Results The intensity of T1-weighted signal increased, the intensity of T2-weighted signal increased and the intensity of signal intensity increased in NR group. The changes of MRI in DR group were lower than those in NR group. The content of EB in brain tissue of DR group was significantly increased at 6 h, The expression of VEGF decreased at 1 week and 1 month and 6 h after irradiation (P <0.05 or 0.01). Conclusion The use of diazepam before irradiation can reduce the permeability of blood-brain barrier in radiation-induced brain injury by decreasing the expression of VEGF in brain tissue, which may have a protective effect on radiation-induced brain injury.