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目的观察苯二氮卓受体对放射性脑损伤大鼠氧自由基的影响。方法210只SD大鼠随机分为7组,每组30只,D-R组:照射前30min腹腔注射地西泮5mg/kg;F-R组:照射前30min腹腔注射氟马西尼0.025mg/kg;DF-R组:照射前30min腹腔注射地西泮5mg/kg,照射前15min腹腔注射氟马西尼0.025mg/kg;N-R组:照射前未用药;D-SR组:假照射前30min腹腔注射地西泮5mg/kg;F-SR组:假照射前30min腹腔注射氟马西尼0.025mg/kg;N-SR组:假照射前未用药。所有照射组建立清醒状态下大鼠放射性脑损伤模型。各组分别于照射(或假照射)前即刻、照射后6h、1d、1周和1个月时测定脑组织中超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量的变化。结果N-R、F-R、DF-R组照射后脑组织SOD活力较D-R组减弱,MDA含量较D-R组增加(P<0.05)。结论在照射前使用地西泮可增强脑组织SOD活力,降低脑组织中MDA含量,氟马西尼在用药后可以拮抗地西泮的作用,苯二氮卓受体对放射性脑损伤大鼠的自由基损伤有一定的防护作用。
Objective To observe the effects of benzodiazepine receptor on oxygen free radicals in rats with radiation brain injury. Methods 210 Sprague-Dawley rats were randomly divided into 7 groups (30 rats in each group): DR group: 5 mg / kg diazepam intraperitoneally 30 min before irradiation; FR group: 0.025 mg / kg flumazenil intraperitoneally 30 min before FR; Group R: intraperitoneal injection of diazepam 5 mg / kg 30 min before irradiation, intraperitoneal injection of flumazenil 0.025 mg / kg 15 min before irradiation; NR group: no drug before irradiation; D-SR group: In the F-SR group, flumazenil 0.025 mg / kg was injected intraperitoneally 30 min before sham irradiation. In the N-SR group, no drug was administered before sham irradiation. All irradiation group established a rat brain radiation brain injury model. The changes of superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in brain tissue were measured at 6h, 1d, 1w and 1 month after irradiation (immediately before or immediately after sham irradiation). Results Compared with D-R group, the activity of SOD in brain tissue of N-R, F-R and DF-R groups was weakened and MDA content increased (P <0.05). Conclusions The use of diazepam before irradiation enhances the activity of SOD in brain tissue and decreases the content of MDA in brain tissue. Flumazenil can antagonize the effect of diazepam after administration, and the effect of benzodiazepine receptor on radiation-induced brain injury in rats Free radical damage has a protective effect.