EFFECTS OF THROMBIN PRE-TREATMENT ON CATHEPSIND, BECLIN-1 AND VEGF OF CEREBRAL HAEMORRHAGE MODEL IN RATS

Objective: To investigate the effects of thrombin pre-treatment on CathepsinD, Beclin-1 protein and VEGF of a model of cerebral haemorrhage in rats. Methods: 72 SD rats were randomly divided into a normal control group, a model group and a TPC group by a numerical method. Each group was divided into subgroups of 3 h, 6 h, 12 h,1 d, 3 d and 7 d, with 4 rats in each group. Cerebral haemorrhage model was made by intracerebral stereotactic injection of collagenase. 1U thrombin was stereotactically injected into the right striatum in TPC group 1d before the model was made. The expression levels of CathepsinD, Beclin-1 and VEGF were determined by immunohistochetnisny. The water content of brain tissue was measured on day 3 and 7 after cerebral haemorrhage. Neurological defects of rats in each group were scored at 3 h, 6 h, 12 h, 1 d, 3 d and 7 d after cerebral haemorrhage. Results: Compared with the normal control group, the amount of CathepsinD and Beclin-1 positive in the TPC group and the model group reached a peak one day after intracerebral haemorrhage, but the amount of CathepsinD and Beclin-1 positive in the TPC group was more significant (P<0.05). The amount of CathepsinD and Beclin-1 positive in the brain tissue on day 3 after intracerebral haemorrhage gradually decreased; and the decrease was more significant in the TPC group than in the model group (P<0.05). After modelling, the amount of VEGF positive in the model group and TPC group was significantly higher than that in the normal group (P<0.05), but the increase in the TPC group was more significant than that in the model group. Compared with the normal group, the water content of brain tissue in the other two groups increased significantly on the third day (P<0.05), and decreased on the seventh day (P<0.05). The TPC group showed a more significant decrease than the model group (P<0.05). The neurological defect scores of the model group and the TPC group were significantly increased at 6h, 12h and Id after modelling, and decreased at 3d after bleeding. Compared with the model group, the neurological defect scores of the TPC group were significantly decreased at 7d (P<0.05). Conclusion: Thrombin pre-treatment can down-regulate the expression of CathepsinD and Beclin-1 protein, up-regulate the expression of VEGF, reduce cerebral oedema, reduce secondary damage to brain tissue, and promote the neurological function recovery after intracerebral haemorrhage.