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目的:观察新生大鼠缺氧缺血性(HI)脑损伤后NO水平的变化,探讨单唾液酸四己糖神经节苷脂(GM1)对NO水平的影响。方法:选择新生7日龄Sprague-Dawley大鼠108只,随机分为三组:缺氧缺血组(HI组,36只),假手术对照组(Control组,36只),缺氧缺血+神经节苷脂组(GM1组,36只)。采用结扎右侧颈总动脉并吸入低氧混合气体制备HIBD模型。采用镀铜镉还原法测定血浆一氧化氮(NO)水平。结果:Control组、HI组、和GM1组新生大鼠血浆NO-2/NO-3含量分别为(41.6±8.9)、(60.9±14.7)和(43.8±10.6)μmol/L。HI组明显高于对照组和GM1组(P<0.05);GM1组与对照组比较,无明显差异(P>0.05)。结论:GM1能抑制新生大鼠缺氧缺血性(HI)脑损伤后NO生成,对缺氧缺血(HI)新生大鼠的脑具有保护作用。
Objective: To observe the changes of NO level in neonatal rats after hypoxic-ischemic (HI) brain injury and to explore the effect of GM1 on the level of NO. Methods: One hundred and eight newborn 7-day-old Sprague-Dawley rats were randomly divided into three groups: hypoxic-ischemic group (HI group, 36 rats), sham operation control group (36 rats), hypoxic- + Ganglioside group (GM1 group, 36). HIBD model was prepared by ligating right common carotid artery and inhaling hypoxia mixed gas. Plasma nitric oxide (NO) level was measured by copper-cadmium reduction. Results: The levels of NO-2 / NO-3 in control group, HI group and GM1 group were (41.6 ± 8.9), (60.9 ± 14.7) and (43.8 ± 10.6) μmol / L, respectively. HI group was significantly higher than the control group and the GM1 group (P <0.05); GM1 group and the control group, no significant difference (P> 0.05). CONCLUSION: GM1 can inhibit NO production in neonatal rats with hypoxic-ischemic (HI) brain injury and protect the brain of hypoxic-ischemic (HI) neonatal rats.