Expression of Ephrin-B2 after focal cerebral ischemia in rats.
10.3969/j.issn.1672-7347.2014.05.003
- Author:
Hui XIAO
1
,
2
;
Wenping GU
;
Qidong YANG
;
Xuehui ZENG
Author Information
1. Department of Neurology , Xiangya Hospital, Central South University, Changsha 410008
2. Department of Neurology, Changsha Municipal Central Hospital, Changsha 410004, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Astrocytes;
metabolism;
Brain;
pathology;
Brain Ischemia;
metabolism;
Cerebral Cortex;
metabolism;
Ephrin-B2;
metabolism;
Infarction, Middle Cerebral Artery;
Ischemic Attack, Transient;
Neurons;
metabolism;
Rats;
Rats, Sprague-Dawley;
Reperfusion Injury;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2014;39(5):452-457
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the expression profile of Ephrin-B2 in the ischemic penumbra after transient focal cerebral ischemia in rats, and to clarify the mechanism of Ephrin-B2 triggering angiogenesis.
METHODS:Sprague-Dawley rats were randomly divided into a normal group, a sham operation group and ischemic-reperfusion 1, 3, 7, 14, and 28 d groups. Suture-occluded method was used to establish the focal middle cerebral artery occlusion model and the ischemic brain was reperfused 2 h after the occlusion. Western blot and quantitative real-time reverse-transcription polymerase chain reaction were used to detect the dynamic expression profile of Ephrin-B2 in the penumbra cortex. Double immunofluorescence was used to speculate the location and the co-expression of Ephrin-B2 in blood vessels, neurons and astrocytes. Microvessel density was quantified by the number of CD31+ cells. Rats were subjected to neurologic functional tests by modified neurological severity scores (mNSS) before sacrifice.
RESULTS:Compared with the sham group, Ephrin-B2 protein and mRNA level of the penumbra cortex in the ischemic group increased 3 days (P<0.05) after the reperfusion, peaked at day 7 and 14 (P<0.01), and declined at day 28. Double immunofluorescence indicated that Ehprin-b2 was expressed in the neurons, blood vessels and astrocytes; mNSS peaked at day 7, and gradually declined at day 14. The microvessel density of penumbra cortex in the ischemic group increased 3 days (P<0.05) after the reperfusion, peaked at day 14 (P<0.01), and gradually declined at 48 h.
CONCLUSION:Cerebral ischemia reperfusion induces the over-expression of Ephrin-B2, with a dynamic trend, suggesting that Ehprin-b2 may improve post-stroke functional recovery by enhancing angiogenesis and neurogenesis.
