Protective effects of ischemic preconditioning on cerebral ischemic-reperfusion in rats
10.13699/j.cnki.1001-6821.2017.08.008
- VernacularTitle:脑缺血预处理对大鼠脑缺血再灌注损伤的保护作用
- Author:
Huan-Huan WANG
1
;
Qian XUE
;
Yu-An ZOU
;
Jing-Fang WU
Author Information
1. 河北北方学院,河北张家口075000
- Keywords:
ischemic preconditioning;
reperfusion injury;
nuclear factor E2 related factor 2;
quinone oxidoreductase 1 signaling pathway;
oxidative stress
- From:
The Chinese Journal of Clinical Pharmacology
2017;33(8):699-702
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effects of cerebral ischemic precondition (CIP) on ischemia reperfusion (I/R) and observe the impact of CIP on nuclear factor E2 related factor 2 (Nrf2) and quinone oxidoreductase 1 (NQO-1) signaling pathway.Methods Male,healthy Sprague-Dawley rats were used and randomly assigned to three groups:Sham group,model group (middle cerebral artew occlusion,MCAO),experimental group (cerebral ischemic preconditioning,CIP).The expression of Nrf2 was analyzed by immunohistochemisty.The mRNA expression of Nrf2 and NQO-1 were measured by the Quantitative real-time polymerase chain reaction method.The content of malonaldehyde (MDA) and activity of superoxide dismutase (SOD) were determine by thiobarbituric acid assay and water-soluble tetrazolium-1 assay,respectively.Results The number of Nrf2 nuclear positive cells,reached the peak at 24 h.The number of nuclear positive cells in experimental group and model group were (78.33 ± 10.15),(63.50 ±6.66).Compared with the model group,the number of nuclear positive cells was more in experimental group,the difference was statistically significant (P ＜ 0.05).The expression of Nrf2,NQO-1 mRNA,reached the peak at 24 h.The expression of Nrf2 in experimental group and model group were (3.07 ± 0.55),(2.41 ±0.61).The expression of NQO-1 in experimental group and model group were (3.78 ± 0.52),(2.73 ±0.76),the difference was statistically significant(P ＜0.05,P ＜0.01).The content of MDA was reached the peak at 24 h.The content of MDA in experimental group and model group were (25.43 ± 8.68),(39.91 ± 7.10) nmol,mg-1 prot.The content of MDA was higher in model group than that in experimental group,the difference was statistically significant(P ＜ 0.05).The activity of SOD was decreased after ischemia at 6 h,reached the peak at 24 h.The activity of SOD experimental group and in model group at 24 h were (269.83 ± 42.41),(189.50 ± 37.57) U · mg-1 prot.The activity of SOD was higher in experimental group than that in model group at 24,48 h,the difference was statistically significant (P ＜ 0.05).Conclusion CIP regulate the expression of downstream products of oxidation stress by Nrf2/ARE signaling pathway to protect brain tissue damage caused by cerebral ischemia repeffusion.
