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目的探讨3日龄未成熟大鼠缺氧缺血性脑损伤后脑白质中iNOS的表达变化规律,研究iNOS在早产儿脑损伤发病机制中的作用,为干预治疗打下理论基础。方法 92只体质量6.5～10.5 g新生3日龄SD大鼠,随机分为实验组(缺氧缺血)50只和对照组(假手术)42只,实验组死亡10只,对照组死亡2只,故进入实验的两组均为40只。实验组大鼠右侧颈总动脉结扎,术后予以低氧(6%O2+94%N2)处理4 h,以建立动物模型。对照组仅分离右侧颈总动脉,不予结扎和缺氧处理。术后12、24、48、72 h及7 d处死8只大鼠取脑组织制备光镜石蜡标本。iNOS的表达采用免疫组化方法。采用全自动图像分析系统分析iNOS阳性单位表达的AU值。结果对照组胼胝体、脑室周围白质无iNOS蛋白的免疫阳性表达。实验组缺氧缺血12 h iNOS在胼胝体和脑室周围白质表达开始增加,72 h达高峰,7 d仍有表达,组间各时间点比较差异均有统计学意义(P<0.05)。与对照组比较,缺氧缺血12、24、48、72 h及7 d iNOS在胼胝体和脑室周围白质表达差异有统计学意义(P<0.05)。结论未成熟大鼠缺氧缺血性脑损伤中,iNOS蛋白的表达于缺氧缺血12 h开始增加,于72 h达到高峰,7 d仍有表达,说明iNOS在其发病机制中有一定作用。
Objective To investigate the changes of iNOS expression in white matter of hypoxic-ischemic brain damage in 3-day-old immature rats, and to study the role of iNOS in the pathogenesis of premature infant brain damage and lay a theoretical foundation for interventional therapy. Methods Ninety-two newborn SD rats aged 6.5-10.5 g were randomly divided into experimental group (hypoxic-ischemic) 50 and control group (sham) 42, experimental group 10 and control group 2 Only, so the two groups into the experiment are 40. The right common carotid artery was ligated in the experimental group and was treated with hypoxia (6% O2 + 94% N2) for 4 hours after operation to establish an animal model. The control group only isolated the right common carotid artery, not ligation and hypoxia. Eight rats were sacrificed at 12, 24, 48, 72 h and 7 d after operation. Light microscope paraffin was prepared. The expression of iNOS was detected by immunohistochemistry. AU value of iNOS positive units was analyzed by automatic image analysis system. Results In the control group, there was no immunostaining positive expression of iNOS protein in corpus callosum and periventricular white matter. In the experimental group, the expression of iNOS in corpus callosum and periventricular white matter began to increase 12 h after hypoxia-ischemia and peaked at 72 h, and still remained at 7 d after hypoxia-ischemia (P <0.05). Compared with the control group, the expression of iNOS in corpus callosum and periventricular white matter at 12, 24, 48, 72 h and 7 d after hypoxia-ischemia were significantly different (P <0.05). Conclusions The expression of iNOS protein in hypoxic-ischemic brain damage of immature rats began to increase 12 hours after hypoxia-ischemia, peaked at 72 hours and remained at 7 days, indicating that iNOS plays a role in its pathogenesis .