Protective effect of Apelin-13 on focal cerebral ischemia-reperfusion injury in rats
- VernacularTitle:Apelin-13对大鼠局灶性脑缺血-再灌注损伤的保护作用
- Author:
Guangyong WU
1
;
Liang LI
;
Daguang LIAO
;
Zhifei WANG
Author Information
1. 中南大学湘雅三医院神经外科
- Keywords:
apelin-13;
brain ischemia-reperfusion injury;
malondialdehyde;
superoxide dismutase;
extracellular regulated kinase1/2
- From:
Journal of Southern Medical University
2015;(9):1335-1339
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect of Apelin-13 on focal cerebral ischemia-reperfusion injury in rats. Methods Focal transient cerebral ischemia-reperfusion injury was induced in male SD rats using modified suture occlusion technique. The rats were randomly divided into 5 groups: Sham group, Model group, Apelin-low dose (A) group, Apelin-middle dose (B) group and Apelin-high dose (C) group. Apelin-13 was injected into lateral cerebral ventricle, and the neurological function score, brain edema, infarct volume, apoptosis, malondialdehyde (MDA), superoxide dismutase (SOD) and extracellular regulated kinase1/2 (ERK1/2) protein were measured. Results Neurological function scores, percentage of brain water content, infarct volumes and TUNEL-positive cells in B and C groups were lower than those in Model group (P<0.05). The level of MDA in the tissue bomogenate of brain tissue in the surrounding area of ischemia of B and C groups was lower than that of Model group, while the activity of SOD was higher (P<0.05). There was no significant difference in ERK1/2 protein expression among the groups (P>0.05). P-ERK1/2 increased in Model group and A, B, and C groups compared with Sham group (P<0.05), and that of A, B, and C group was higher than that of Model group (P<0.05). Conclusion Apelin-13 may play an important role by inhibiting oxidative stress to protect against focal cerebral ischemia-reperfusion injury; ERK1/2 signaling pathway may be involved in the protective mechanism of Apelin-13.