Abstract:

Objective      To investigate expressions and relations of p38MAPK, NF-κB and ICAM-1 in the origin and progression of CVS(Cerebral vasospasm) in SAH(Subarachnoid hemorrhage) rabbits. Methods      40 New Zealand pure rabbit were divided into the control groups, the anti-ICAM-1 monoclone antibody treatment group, the NF-κB antagonist treatment group, and the p38MAPK inhibiting group. Models of SAH and CVS were established via double blood injection into the major cistern and the basilar artery(BA) was dissected. Morphological methods, immunohistochemistry and hybridization in situ were employed to observe the variance of the basilar artery and dynamic expressions of p38MAPK, NF-κB and ICAM-1 in the wall of the BA. Results       Stenosis of the BA appeared in the control group, but not in other groups. Intensive expressions of p38MAPK, NF-κB and ICAM-1 were identified by immuno-histochemistry in tunica intima and subintima of BA vessel walls in the control group. In the group treated with the p38MARK inhibitor, expressions of p38MAPK, NF-κB and ICAM-1 were localized in tunica intima and subintima, and expression was slight. After the NF-κB antagonist was administered, expressions of p38MAPK, NF-κB and ICAM-1 were slight in tunica intima and subintima, however, expression of p38MARK appeared in tunica media. In the anti-ICAM-1 monoclone antibody treatment group, there were expressions of p38MAPK and NF-κB in both tunica intima and media,while slight expression of ICAM-1 was observed only in tunica intima and media. Results of hybridization in situ were similar to those of immune-histochemistry. Conclusion       Inflammation reaction induced by ICAM-1, which is regulated by p38MAPK and NF-κB, exists in rabbit BA, and plays an important role in the origin and progression of CVS.

Key words: Subarachnoid hemorrhage; Cerebral vasospasm; p38 Mitogen-activated kinase protein; Nuclear transcription factor-κB; Intercellular adhesion molecule-1