Kallikrein gene transfer promotes recovery of regional cerebral blood flow after cerebral ischemia/reperfusion injury in rats
10.3760/cma.j.issn.1671-8925.2008.10.011
- VernacularTitle:Kallikrein基因转导对脑缺血再灌注后局部血流灌注恢复的作用
- Author:
Rui-Yan L(U)
1
;
Qing-Yu SHEN
;
Lian-Hong YANG
;
Mei LI
;
Yi-Dong WANG
;
Ying PENG
Author Information
1. 中山大学附属第二医院
- Keywords:
Cerebral ischemia/reperfusion,Adenovirus mediated;
Kallikrein;
Vascularendothelial growth factor
- From:
Chinese Journal of Neuromedicine
2008;7(10):1013-1018
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects ofkallikrein gene transfer on microvascularproliferation around the cerebral infarct and on the recovery of regional cerebral blood flow (rCBF)following ischemia/reperfusion injury in rats. Methods The rats with cerebral ischemia/reperfusioninjury induced by middle cerebral artery occlusion (MCAO) were randomly assigned into blank controlgroup, saline group, and pAdCMV-HTK treatment group and received corresponding injections into thetissues around the infarct area. Each group was divided into 3 subgroups (n=10) for observation at 12, 24and 72 h after the treatment. The neurological deficits of the rats before and after the treatment wereevaluated using neurological severity scores (NSS), and the expressions of exogenous human tissuekallikrein (HTK) and vascular endothelial growth factor (VEGF) in the brain tissues were detectedimmunohistochemically. TIC staining was performed to measure the changes in the infarct size.14C-iodoantipyrine tracing technique was used to define the rCBF in the rats. Results Compared tothe blank control group, the cerebral infarct size was significantly reduced in pAdCMV-HTK group 24 hafter the treatment, and was further reduced at 72 h (P<0.05). At 24 h after the treatment, the NSS inpAdCMV-HTK group was significantly lower than that in the blank euntrol and saline groups (P<0.05),and was further reduced at 72 h (P<0.01). After MCAO, the VEGF-positive cells were found mostly inthe cortex and the white matter around the infarct area. The expression of VEGF in pAdCMV-HTK groupwas markedly higher than that in the other two groups at 12, 24, and 72 h after the treatment (P<0.05). Inall the 3 groups, the rCBF around the infarct was slightly decreased as compared to that in thecontralateral hemisphere, pAdCMV-HTK slightly increased the rCBF 12 h after the injection (P>0.05),and significant increase in the rCBF occurred 24 h and 72 h after the injection (P<0.05). ConclusionKallikrein gene transfer following cerebral ischemia/reperfusion injury promotes vascular proliferationaround the infarct and increases the rCBF to reduce the infarct volume and attenuate neurological deficitsin rats.
