CAJ | 학술논문

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3～5 d(生后6～8 d) IGF-1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7～14 d(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48 h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.
목적탐토이도소양생장인자-1(IGF-1)재3일령미성숙대서만성결양결혈뇌손상발병궤제중적작용. 방법 90지3일령SD미성숙대서수궤분위대조조(n=40)화만성결양결혈(HI,n=50)조.대조조부절개경부피부,HI조결찰쌍측경총동맥조성신생대서만성결양결혈뇌손상,채용조직절편소목소-이홍염색화면역조화등방법,관찰미성숙대서뇌손상시소돌효질세포영양인자IGF-1화수체적표체、뇌조직병리변화화백질세포조망.결과 3일령미성숙대서만성결양결혈뇌손상후IGF-1급기수체정현동태변화.HI조재술후3～5 d(생후6～8 d) IGF-1표체양성적세포감소,IGF-1수체표체각유증고추세,변화이변지체화뇌실주위백질부위명현,술후7～14 d(생후10～17d)시축점회복.동시뇌백질출현액화소송、뇌실확대등형태학병리변화,조망세포계수재손상후증다,이48 h최위현저.결론제시IGF-1재3일령미성숙대서만성결양결혈뇌손상적발병궤제중구유중요작용,위조산인뇌손상적방치제공료실험의거.
Objective This study examined the expression of insulin-like growth factor-1(IGF-1)and its receptor in 3-day-old premature rats with chronic hypoxic ischemic brain damage (HIBD) and investigated the role of IGF-1 in the pathogenesis of this disease.Methods Ninety 3-day-old Sprague-Dawley rats were randomly assigned into a Control group (n =40) and a Hypoxic-ischemic group (HI, n = 50). HI was induced through bilateral common carotid artery ligation. The Control group was only sham-operated. Hematoxylin and eosin staining, TUNEL immunofluorescence staining and immunohistochemistry ways were used to investigate the expression of IGF-1 and its receptor, morphological changes of brain tissues and cell apoptosis of brain white matter. Results The expression of IGF-1 decreased in 3-5 days after HI, but that of its receptor increased in the HI group. The expression changes were most significant at corpus callosum and peri-ventricular white matter and recovered progressively in 7-14 days after HI. After 7 days of HI, the brain white matter presented with morphological changes such as rarefaction, liquefaction and lateral ventricular enlargement. Apoptotic cells in deep white matter increased after HI, and peaked at 48 hrs. Conclusions IGF-1 may play an important role in the pathogenesis of chronic HIBD in 3-day-old premature rats. This study provides an experimental basis for the prevention and treatment of HIBD in premature infants.