| Objective: Hypoxic-ischemic encephalopathy (HIE) is one fatal disease to the health of neonatus and often has much sequel to affect their development. Scholars have studied HIE for many years, they believe its pathogenesis is still unclear and referring to some paths, such as a lot of release of excitatory amino acid (EAA) or the failure of energy and apoptosis which is the main style to delayed neuron death. While HIE is short of effective therapical method yet. Today we know Insulin-like growth factor-1 (IGF-1) which maybe rescue heart and renes from ischemia is an important protein to the development and repairment of brain, but within the infarct and in surrounding areas, strong IGF-1 immunoreactivity was not detected after hypoxia- ischemia until 3 days. This research use rat model to study histological feature and the level of Glutamate (Glu) , apoptosis and the expression of Bcl-2 protein in the hemisphere ipsilateral to the injury, also study blood glucose and blood urea nitrogen (BUN) and creatine kinase (CK) in serum and observe their changes after therapy with IGF-1.Methods: 128 7-day-old Wistar rats were randomlydivided into: normal control group; sham-operated control 24h (h: hour), 48h, 72h groups; HIBD ( HIBD: hypoxic-ischemic brain damage) 24h, 48h, 72h groups; HIBD treated with 0.2mg/kg RH-IGF-1 24h, 48h, 72h groups and 0.066 mg/kg RH-IGF-1 24h, 48h, 72h group; NS (NS: saline) control 24h, 48h, 72h groups, respectively. There were 8 rats in each group. HIBD model was induced by ligating the left common carotid artery of rats and being exposed to 8% oxygen for 2 hours. Right after hypoxic-ischemic insult, IGF-1 or NS were injected intraperitoneally. Rats were killed at the directed time and brain tissue, serum were prepared. Using hematoxylin-eosin (HE) or Alican Blue staining and light-microscopy observed the histological feature of the left brain. Level of Glu was measured by high-performance liquid chromatography (HPLC) assay, level of apoptosis and expression of Bcl-2 protein were examined by flow cytometry (FCM). Level of glucose and BUN and CK in serum were measured with biological-chemical methods. Rats behavior were also observed and so on.Results 1. At the opening of the research, there are 128 rats, but 14 rats died during and after hypoxia-ischemia, so 114 rats are left in the research. During hypoxia, rats first excite and then have lip cyanosis and tremble which last about 30 minutes, then get depressed. 2. At the opening of the research, each rat is healthy. 1 hourafter hypoxia, 32 rats which belong to normal control and sham-operated groups are still healthy, while in the 85 rats which bare hypoxic-ischemic injury, 54 rats couldn't turn themselves over and 69 rats become levogirating when their tails are gripped. There are 41 rats couldn't turn themselves and become levogirating when their tails are gripped. 3. Under light-microscope, the sections of each HIBD group's brain tissue exhibits degeneration and necrosis of neurons, diminishing and loss of dendrite and Nissl's bodies in neuron, obliterative vascular and gliosis, which become much severer as time is longing. 4. Level of Glu in HIBD 48h group is significantly higher than that in sham-operated 48h group, by student t test (t=5.087,P<0.05). 5. Levels of apoptosis in every HIBD groups are significantly higher than those in sham-operated groups of the same time, respectively, by student t test (t=8.442,24.637 ,37.574, P<0.05). Compared between HIBD groups, level of apoptosis in HIBD 48h group is significantly higher than that in HIBD 24h group, by one- way ANOVA (P<0.05); while level of apoptosis in HIBD 72h group is a little higher than that in HIBD 48h group (P>0.05). 6. ⑴ The number of dendrite and Nissl's bodies in neuron get more in RH-IGF-1 treated groups'sections. ⑵ Levels of Glu in every RH-IGF-1 treated 48h groups are significantly less than that in NS control group of the same time, respectively,by one- way ANOVA (F=13.258, P<0.05). ⑶Levels of apoptosi... |
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