目的:观察雄激素干预缺氧缺血性脑病新生大鼠后,鼠脑匀浆中超氧化物歧化酶活性和丙二醛含量的变化。 方法:实验于2004-02在西安交通大学第二医院完成。选择7d龄一级SD大鼠56只。随机抽签法分成假手术对照组8只、缺氧缺血性脑损伤+生理盐水组24只、缺氧缺血性脑损伤+雄激素组24只,按照取材时间的不同,缺氧缺血性脑损伤+生理盐水组和缺氧缺血性脑损伤+雄激素组又分为缺氧缺血后6,24,48h 3个时间点,每个时间点8只。制备缺氧缺血性脑损伤模型,取颈正中切口,游离左颈总动脉,结扎并缝合切口,恢复2~3h后置于约5L自制常温常压密闭容器中,以1.0~2.0L/min的速度输入含体积分数0.08的氧气和体积分数0.92的氮气的混合气体,约2.5h后取出。假手术组仅做颈正中切口,游离左颈总动脉,但不结扎。缺氧缺血性脑损伤+雄激素组在缺氧缺血后立即给予腹腔注射丙酸睾丸酮25mg/kg;缺氧缺血性脑损伤+生理盐水组给予等量生理盐水作对照。然后分别于缺氧缺血性脑损伤后6,24,48h后断头取脑制作脑匀浆,以硫代巴比妥法测定丙二醛含量;黄嘌呤氧化酶发光法测定超氧化物歧化酶。 结果:在实验过程中,缺血性脑损伤+生理盐水组死亡7只;缺血性脑损伤+雄激素组死亡4只;假手术组无死亡。故假手术组8只、缺血性脑损伤+生理盐水组17只、缺血性脑损伤+雄激素组20只大鼠进入结果分析。①假手术组脑组织匀浆中超氧化物歧化酶活性为(60.67±7.26)kNU/g;缺氧缺血性脑损伤+生理盐水组缺氧缺血后6h超氧化物歧化酶活性开始降低,24h降至最低值,与假手术组比较差异均有显著性意义(P〈0.05),48h后逐渐恢复后仍低于正常水平,与假手术对照组比较差异无显著性意义(P〉0.05);缺氧缺血性脑损伤+雄激素?
AIM: To explore the effect of androgen intervention on the changes of superoxide dismutase (SOD) activity and malonaldehyde (MDA) content in brain homogenate of neonatal rat for hypoxic-ischemic brain damage (HIBD) model. METHODS: The experiment was carried out in the Second Hospital of Xi'an Jiaotong University in February 2004. A total of 56 SD rats of 7 days old were divided into three groups according to random sampling rule: sham operated group (n=8), HIBD control group (n=24) and androgen group (n =24). And the latter two groups were assigned into three subgroups equally, 8 rats at each time point (6, 24 and 48 hours after hypoxia and ischemia). HIBD model was induced by making carotid median incision, liberating left common carotid artery and then being sutured. After 2-3 hours of recovery, the mixture gas of O2 in 0.08 volume fraction and N2 in 0.92 volume fraction was infused into the hermetic container at normal temperature and normal pressure at the velocity of 1.0-2.0 L per minute, and was taken out 2.5 hours later. In sham operated group, there was no deligation. In androgen group, intraperitoneal injection of testosterone propionate (25 mg/kg) was given immediately after hypoxia and ischemia (HI). While saline of equal volume was given in HIBD control group. The changes of SOD and MDA level in brain homogenate were observed with xanthine oxidase luminescence and thiobarbituric acid at 6, 24 and 48 hours after HIBD. RESULTS: There were 11 deaths during experiment, including 7 ones in control group and 4 ones in androgen group, therefore, 8 rats of sham operated group, 17 rats of control group and 20 rats of androgen group were involved in the result analysis. ① The SOD activity of brain homogenate in sham operated group was (60.67±7.26) kNU/g; The SOD activity on HIBD control group began reduction at 6 hours after HI, reached the minimum at 24 hours (P 〈 0.05), and steadily raised at 48 hours but was still below that of sham operated grou