The Study On P53 Protein Expression In The Infant-rats With Hypoxic-ischemia Brain Damage

Object: The study was carried out to explore whether or not p53 protein expression in hypoxic-ischemia brain damage (HIBD) and to understand the mechanism of HIBD by determining the changes of content of nitric oxide (NO),nitric oxide synthase (NOS) ,superoxide dismutase(SOD). Method: The models of HIBD in infant-rats were made by the hypoxic-ischemia way of Hu zhi-bing .The infant-rats were divided at randow into two groups. Biochemical index group (group one ) and the p53 protein and pathological detecting group (group two). The rats in group one were divided at random into four subgroup,each with 10. (1) Control subgroup (operated but brain tissue were not hypoxic-ischemia).(2) HIBD subgroup (hypoxic-ischemia). (3) Monosialogangliside (GM1) subgroup (GM1:30mg/kg·time,abdominal injection, five times, hypoxic-ischemia). (4) citicoline sodium subgroup (citicoline sodium:40mg/kg·time, abdominal injection, five times, hypoxic-ischemia ).the subjects were killed 24h after hypoxic-inchemia and detected biochemical index. The rats in group two who were divided at random into four subgroup, each with 10.(so same as group one).were investigated the changes of expression of p53 protein and performed pathological examines. Result: 1. In group one, compared with HIBD subgroup, there were obvious reduce of the content of NO,NOS and marked increase of SOD in the brain tissues of infant-rats in control subgroup. 2. There is significant difference between control subgroup and hypoxic-ischemia subgroup about Expression of p53 protein. There were the disorder of cortical cell structure, arrange and hyperchromatio of nucleus cell and interstitial in HIBD subgroup. In control subgroup, the cortical cell Structure, arrange is in order.by treatment of GM₁ and citicoline sodium, the changes of hypoxic-ischemia brain damage trend to better. Condusion: NO and free radicals are significant to the pathogenesis of hypoxic-ischemia brain damage and induce the expression of p53 protein.GM₁ and citicoline sodium play a role of protecting hypoxic-ischemia brain damage.