2010Zhongguo naoxueguanbing zazhiRequires access

Study of dynamic expression of NF-κB and ICAM-1 after cerebral ischemic preconditioning

Jian Chong-don

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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 neuro-ethological score, infarct volume ratio and expression of NF-kB and ICAM-1 in the ischemic region at the corresponding time points were observed.Results ①The 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) .②The 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. ③The 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.

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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 neuro-ethological score, infarct volume ratio and expression of NF-kB and ICAM-1 in the ischemic region at the corresponding time points were observed.Results ①The 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) .②The 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. ③The 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.

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Available 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 neuro-ethological score, infarct volume ratio and expression of NF-kB and ICAM-1 in the ischemic region at the corresponding time points were observed.Results ①The 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) .②The 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. ③The 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.

Key concepts: Ischemic preconditioning, Medicine, Ischemia, Internal medicine, ICAM-1, Cardiology, Anesthesia, Cell adhesion molecule

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