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目的探讨胰岛素样生长因子-1(IGF-1)在3日龄未成熟大鼠慢性缺氧缺血脑损伤发病机制中的作用。方法90只3日龄SD未成熟大鼠随机分为对照组(n=40)和慢性缺氧缺血(HI,n=50)组。对照组仅切开颈部皮肤,HI组结扎双侧颈总动脉造成新生大鼠慢性缺氧缺血脑损伤,采用组织切片苏木素-伊红染色和免疫组化等方法,观察未成熟大鼠脑损伤时少突胶质细胞营养因子IGF-1和受体的表达、脑组织病理变化和白质细胞凋亡。结果3日龄未成熟大鼠慢性缺氧缺血脑损伤后IGF-1及其受体呈现动态变化。HI组在术后3～5d(生后6～8d)IGF1表达阳性的细胞减少,IGF-1受体表达却有增高趋势,变化以胼胝体和脑室周围白质部位明显,术后7～14d(生后10～17d)时逐渐恢复。同时脑白质出现液化疏松、脑室扩大等形态学病理变化,凋亡细胞计数在损伤后增多,以48h最为显著。结论提示IGF-1在3日龄未成熟大鼠慢性缺氧缺血脑损伤的发病机制中具有重要作用,为早产儿脑损伤的防治提供了实验依据。
Objective To investigate the role of insulin-like growth factor-1 (IGF-1) in the pathogenesis of chronic hypoxic-ischemic brain damage in 3-day-old immature rats. Methods 90 immature SD rats of 3 days old were randomly divided into control group (n = 40) and chronic hypoxic-ischemic (HI, n = 50) groups. In the control group, only the skin of the neck was excised. In the HI group, bilateral common carotid arteries were ligated into the common carotid artery to induce chronic hypoxic-ischemic brain damage in neonatal rats. Tissue sections were stained with hematoxylin-eosin and immunohistochemistry to observe immature rat brain The expression of IGF-1 and receptor of oligodendrocyte, injury of pathology and the apoptosis of white matter cells were observed. Results The IGF-1 and its receptors in 3-day-old immature rats showed dynamic changes after chronic hypoxic-ischemic brain damage. The number of IGF1 positive cells in HI group decreased from 3 to 5 days after operation (6 to 8 days after birth), while the expression of IGF-1 receptor increased with the increase of corpus callosum and periventricular white matter. After 7 to 14 days After 10 ~ 17d) gradually recovered. At the same time white blood cells appeared liquefied loosening, ventricular enlargement and other morphological changes, apoptotic cell count increased after injury, the most significant 48h. Conclusions IGF-1 plays an important role in the pathogenesis of 3-day-old immature rats with chronic hypoxic-ischemic brain damage and provides an experimental basis for the prevention and treatment of brain injury in preterm infants.