Study of dynamic expression of NF-κB and ICAM-1 after cerebral ischemic preconditioning
10.3969/j.issn.1672-5921.2010.07.007
- Author:
Bing-Song LIANG
1
Author Information
1. Department of Neurology
- Publication Type:Journal Article
- Keywords:
Inflammatory reaction;
Intercellular adhesion molecule 1;
Ischemic preconditioning;
Nuclear factor;
Rats
- From:
Chinese Journal of Cerebrovascular Diseases
2010;7(7):369-372
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To study the roles of nuclear factor (NF-kB) and intercellular adhesion molecule 1 (ICAM-1) in cerebral ischemic preconditioning induced brain ischemic tolerance. Methods: A total of 100 clean rats were randomly allocated into 4 groups: control, ischemic, preconditioning, and ischemic preconditioning groups. Both focal and ischemic preconditioning models were induced. The neuroethological score, infarct volume ratio and expression of NF-kB and ICAM-1 in the ischemic region at the corresponding time points were observed. Results: Circled digit one The neurological deficit score in the ischemic group was higher than that in the ischemic preconditioning group. The cerebral infarction volume ratio was higher than that in the ischemic preconditioning group (28.6 ± 3.2% vs. 16.2 ± 3.8%, t = 2.668 [P < 0.05]), and there were significant differences (P < 0.05). Circled digit two The number of NF-KB positive cells in the ischemic preconditioning group were lower than those in the ischemic group at the same time points, but they were higher than those in the preconditioning group, and there were significant differences (P < 0.05). The peak time of the number of NF-KB positive cells in the ischemic preconditioning group was delayed for 48 hours. Circled digit three The numbers of ICAM-1 positive cells in the ischemic preconditioning group were less than those in the ischemic group at the same time points, but they were higher than those in the preconditioning group, and there were significant differences (P < 0.05). Conclusion: Ischemic preconditioning decreases the expression of NF-KB and ICAM-1 after ischemia. The inhibition of inflammatory reaction may be one of the mechanisms of the ischemic tolerance induced by ischemic preconditioning.
