Abstract:

The aim was to study possible molecular biology mechanism of secondary lesion to perihematom a tissue in intracerebral haemorrhage (ICH) rats by testing HSP70, NF-κB, Bax, Bcl-2 of surrounding tissue of hematoma through immunohistochemistry met hod. Sp rague-Dawley male rats were subjected to ICH models. They were randomly divide d into test groups and control groups. Test groups were divided into 7 subgroups at 1 h, 3 h, 12 h, 24 h, 48 h, and 72 h after ICH, control groups were divided into 3 subgroups at 3 h, 24 h, 72 h after normal saline injection. HSP70, NF-κB, Bcl-2, Bax were tested by immunohistochemistry staining at perihematoma area. Positive cells were picked up by HP1000 high-definition colorful pathology im aging analysis system and compared with the control subgroups. HSP70 and NF-κB expressed the most at the hematoma side at 72 h after surgery (P<0.01); The y demonstrated significant difference among subgroups compared with control subgro ups. Bcl-2 expressed the highest at 12 h after surgery (P<0.01) and Bax at 24 h after injection (P<0.01); Bcl-2 and Bax showed significant difference among subgroups compared with control groups (P<0.01). The result suggests t hat dynamic alternation of HSP70, NF-κB, Bcl-2 and Bax participates and plays an important role in the pathologic process of secondary injury to perihematoma tissue.

Key words: intracerebral haemorrhage, cerebral edema, Bcl-2, Bax, HSP70, NF-&kappa, B