Effect of inhibition of P38MAPK phosphorylation on learning and memory and autophagy in hippo-campus of rats after cerebral ischemic postconditioning
10.3760/cma.j.issn.1674-6554.2018.06.002
- VernacularTitle:抑制丝裂原活化蛋白激酶磷酸化对脑缺血后处理大鼠学习记忆及海马区神经细胞自噬的影响
- Author:
Xiaoyun ZHAO
1
;
Ying HAN
;
Yaning ZHAO
;
Yao LIU
;
Jianmin LI
;
Na DOU
;
Dan LI
Author Information
1. 北理工大学护理与康复学院
- Keywords:
P38MAPK;
Ischemic postconditioning;
Learning and memory;
Autophagy;
Rat
- From:
Chinese Journal of Behavioral Medicine and Brain Science
2018;27(6):487-491
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of ischemic postconditioning on autophagy and learning and memory impairment in rats with ischemia-reperfusion injury by P38MAPK.Methods Ninty-six rats were randomly divided into sham group ( Sham group), cerebral ischemia reperfusion group ( CIR group),cerebral ischemic postconditioning group ( CIP group) and cerebral ischemic postconditioning com-bined with SB203580 group (CIP + SB203580 group),and 24 rats in each group. The rat model of cerebral ischemia was established by Pulsinelli four-vessel occlusion. The learning and memory abilities of rats were measured by Morris water maze. HE staining were used to detect the morphological changes of hippocampal neurons. The phosphorylation of P38MAPK and Beclin-1,LC3-Ⅱexpression were observed by immunohisto-chemistry. Results Compared with the Sham group,the number of crossing the platform decreased(24 h: (3.04±0.20)times),and the escape latency was longer in CIR group(24 h:(58.38±1.52) s) (all P＜0.05). The number of survival neurons reduced (24 h:70.93±1.86),and the expression of P38MAPK,LC3-Ⅱ,Bec-lin-1 in immunohistochemistry were increased in CIR group(all P＜0.05). Compared with CIR group,the number of crossing the platform at each time point increased (24 h:(5.46±0.50)times),the escape latency was shorter (24 h:(52.42±1.53)s),the number of survival neurons increased at each time point(24 h:(83.07±5.30)) and the expression level of P38MAPK decreased in the CIP group,while the expression lev-el of LC3-II,Beclin-1 increased (all P＜0.05).Compared with the CIP group,the number of crossing the plat-form((24 h:(7.13±0.33)times),the escape latency was shorter (24 h:(48.04±1.39)s),the number of survival neurons increased at each time point(24 h:(91.40±1.74)),and the expression of P38MAPK was down-regulated,while the expression of LC3-II,Beclin-1 were up-regulated in CIP +SB203580 group(all P＜0.05). Conclusion Ischemic postconditioning can improve learning and memory impairment in rats with is-chemia-reperfusion injury by P38MAPK regulating autophagy.
