| The occurrence rate of FGR is higher in our country. A large amounts of clinical data have shown that infants of the FGR have many of complications. And the occurrence rate in the brain palsy , intelligence obstacle and unusual nerve behavior of is very high. Several studies have shown that infants of IUGR are at increased risk of the damage of cerebral development. The mechanism resulting in the damage is very complicated . While there are a lot of relevant studies are used in it, human being have limited comprehension about this mechanism as before. Revealing the secrets of the mechanism has important meaning to prevention and cure of cerebral damage.Growth - associated protein 43 ( GAP-43 ) relates closely with the cerebral development, neuron differentiation and the repair of damage. It is a phospho-protien of the nerve terminal membrane which has been thought to be linked to the intelligence for a long time. It is expressed widely in the developing brain and is involved in the establishment of synaptic connections. Many studies on the damage of brain in animal model suggest the expression changes of GAP-43. It plays an important role in the central nervous system growth. GAP-43 can be used as one of the important indexes during the research of nervous development and growth ,in addition ,the repair of damage. As to the relitation about GAP-43 and FGR, there have been not relevant studies in the national and international.In this study, the experimental model of Wigglesworth was used to limit the maternal blood supply to the rat fetus and induce intrauterine growth retardation. We investigated the damage of cerebral development involvement in FGR . In order to looking into the brain damage ,we observed GAP-43 in the rat brain by immunohistochemical staining.Material and methodes1. Animal modelThe experimental model of Wigglesworth was used to limit the maternal blood supply to the rat fetus and induce FGR. On the 17th day of gestation, FGR was induced in rats by ligating the blood supply to the left side of the uterine horn for 30 minutes. The festuses from the uterine vessel ligated side were the fetal growth retarded fetuses and the fetuses from the nonligated side were controls. After this 30 minutes clamping, the group FGR was reperfused again. The pups were taken out on the 20 day of pregnancy by operation, their body weight were measured and brain were gotten.2. Dye and examination for GAP-43The brains were reserved in 10% formaldehyde for 48 -72 hours (4oC) and then these were normaly paraffined. Blocks of the brains were sectionedone in the coronal plane one after another. The thickness of brain piece was 7jxm. Sections from neonatal mouse brain were stained for immunohistochemical studies and were reacted with GAP-43 antibody.About 3-4 sections were gotten from every brain block. Those brain pieces contained dorsal hippocampus and cerebellar of parietal lobe and they were si-miller. Using a x40 objective on the microscope, each delineated area was divided by the computer into small, randomly selected squares and images about GAP-43 were digitized (integrated optical density total) and stored.Results1. The body weightThe mean weight of the ischemic fetuses was 3. 324 + / - 0. 338 ( mean + SD ) g which was significantly lower ( P less than 0.001) than the mean weight of the control fetuses ( 3. 965 +/- 0.3 23 g). FGR models were successfully established in Wistar rats by ligation of the medial the blood supply to one of the uterine artery and vein for 30 minutes.2. The expression of GAP-43Integrated optical density in parietal lobe molecular tier in the ischemic group was 10891. 98 +/-2016. 24,while that in control group was 13510. 12 + / -2790. 28. Significant decrease in Integrated optical density occurred in the ligated group as compared with those of the control group ( P < 0.01).Integrated optical density of CA1 in hippocampus in the ischemic group was 10406. 03 +/ -2016.24 ,while that in control group was 10332. 64 +/ -1904. 25. A little hight... |
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