热休克蛋白干预脑缺血缺氧模型大鼠神经功能及脑组织中 血红素加氧酶1 蛋白的表达.

BACKGROUND: Cerebral ischemia and hypoxia can trigger a series of complex cascade reactions. Due to its complex pathogenesis, there is no ideal drug for the treatment of cerebral ischemia and hypoxia. OBJECTIVE: To investigate the effects of heat shock proteins on heme oxygenase-1 protein expression and neurological function in rats with cerebral ischemia and hypoxia. METHODS: Thirty rats were randomly divided into sham-operated group, model group, heat shock protein 70 group, with 10 rats in each group. Animal models of cerebral ischemia and hypoxia were made in the latter two groups. Rats in the sham-operated group were given no ligation. After modeling, the heat shock protein 70 group was given tail injection of recombinant adenovirus vAd-HSP70 suspension (0.5 mL), once a day for 3 days. The neurological function, oxidation index, water content and infarct area of the three groups were compared. Hematoxylin-eosin staining was used to observe the morphology of the rat brain. Western blot was used to detect the expression of heme oxygenase-1 protein in the rat brain. RESULTS AND CONCLUSION: Compared with the sham-operated group, the neurological function scores in the model group were significantly decreased, while those in the heat shock protein 70 group were significantly increased (P < 0.05). The brain water content and infarct area of rats in the model group were significantly higher than those in the sham-operated group (P < 0.05), and the brain tissue of rats in the model group had significant changes, with scattered cell distribution, significant loss of cells and increased number of necrotic cells. Compared with the model group, the brain water content and infarct area were significantly decreased in the heat shock protein 70 group (P < 0.05) and the morphology of brain tissue was significantly improved (P < 0.05). The expression of heme oxygenase-1 protein in the brain tissue was significantly lower in the model group than the sham-operated group, but was significantly higher in the heat shock protein 70 group than the model group (P < 0.05). To conclude, heat shock proteins can effectively reduce oxidative stress damage, improve neurological function, and decrease cerebral infarct area and brain water content in the rat model of cerebral ischemia and hypoxia. Its mechanism of action may be related to the increase of heme oxygenase-1 protein expression. [ABSTRACT FROM AUTHOR]