Effects of cerebral ischemic preconditioning on receptor for advanced glycation end-products and interleukin-1β in cerebral cortex of rats
10.13699/j.cnki.1001-6821.2017.05.015
- VernacularTitle:缺血预处理对大鼠大脑皮层晚期糖基化终末受体和白细胞介素-1β的影响
- Author:
Jing ZHANG
1
;
Yu-An ZOU
;
Qian XUE
;
Xiao-Hua DONG
Author Information
1. 河北北方学院
- Keywords:
cerebral ischemic preconditioning;
ischemia-reperfusion injury;
advanced glycation end-products;
interleukin-1β
- From:
The Chinese Journal of Clinical Pharmacology
2017;33(5):439-442
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the changes of receptor for advanced glycation end-products (RAGE) and intedeukin-1β (IL-1β) in cerebral cortex of rats after cerebral ischemic preconditioning (CIP) and to further explore the signification of CIP.Methods SPF healthy male SD rats were assigned randomly into 3 group:model Ⅰ group (n =36),model Ⅱ group (n =36),and sham group (n =36).The rats in model Ⅱ group were subjected to 2 hour of right middle cerebral artery occlusion (MCAO) reperfusion with suture-occluded method to establish focal cerebral ischemia reperfusion injury model.Ten miniutes MCAO by suture-occluded was used as model Ⅰ group,72 hours after reperfusion,given the same treatment like the model Ⅱ group.For the sham group,separate the carotid artery only.Each group was divided into 0.5 days,1 day,2 days,3 days,7days total of five time points after reperfusion,6 rats at each time point.After surgery,the infarction volume was evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) staining.The neural behavioral score were measured by Zea Longa assessment criteria.The expression levels of RAGE and IL-1β mRNA were assessed by the method of real-time quantitative polymerase chain reaction.Results Comparison of rats in 1 d after ischemia,the infarct volume in model Ⅰ group was (19.04 ± 1.65) ％ which was lower than model Ⅱ group(34.55 ±4.78) ％,the difference was statistically significant (P ＜ 0.05).Compared with model Ⅱ group,the average neural behavioral scores at each time point were less than 2.2 points in model Ⅰ group,they were significantly reduced (P ＜ 0.05).The expression of RAGE mRNA:The Delta C (T) value of RAGE in the model Ⅰ and model Ⅱ groups were significantly higher than the sham group at that times,reached the peak at the time of 1 d,the Delta C (T) value of the sham group,the model Ⅰ group and model Ⅱ group were 6.56 ±0.08,9.52 ± 0.23,9.89 ± 0.17,which relative expression quantity being calculated were 1.24,9.65,12.47,both decreased with the prolonging of reperfusion time.The Delta C (T) value of the sham group,the model Ⅰ group and model Ⅱ group at 3 d were 6.18 ±0.32,7.87 ±0.36,8.61 ±0.24,the expression levels of model Ⅰ group were significantly lower than the model Ⅱ group at those five time points(P ＜0.05).The expression of IL-1β mRNA:its Delta C (T) value of IL-1β in the model Ⅰ group and model Ⅱ group were both significantly higher than the sham group at 0.5 days,1day,2 days,3days,7days,for example,the Delta C(T) value of the sham group,the model Ⅰ group and model Ⅱ group at 3 days were 7.75 ±0.32,9.94 ±0.18,10.38-±0.27,which relative expression quantity being calculated were 1.09,4.96,6.73,the difference was statistically significant(P ＜0.01),the model Ⅰ group was significantly lower than the model Ⅱ group at those five time points,the Delta C(T) value of the two groups at 0.5 d were 11.84 ± 0.43,12.51 ± 0.36,which relative expression quantity being calculated were 18.51 and 29.45,the expression was descending gradually along with the time (P ＜ 0.05).Conclusion CIP can produce cerebral ischemic tolerance,the down-regulation of RAGE and IL-1β expression may be one of the mechanisms of ischemic tolerance induced by CIP.
