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Expression of Urotensin II During Focal Cerebral Ischemic in Diabetic Rats

Published online by Cambridge University Press:  20 October 2014

Lin Tian
Affiliation:
Department of Pathology, the First Affiliated Hospital of Harbin Medical University, Harbin
Yunqian Li
Affiliation:
Department of Neurosurgery, the First Hospital, Jilin University, Changchun, PR China
Wei Hua
Affiliation:
Department of Pathology, the First Affiliated Hospital of Harbin Medical University, Harbin
Ying Jia
Affiliation:
Department of Pathology, the First Affiliated Hospital of Harbin Medical University, Harbin
Min Zhou
Affiliation:
Department of Pathology, the First Affiliated Hospital of Harbin Medical University, Harbin
Yunhe Gu
Affiliation:
Department of Pathology, the First Affiliated Hospital of Harbin Medical University, Harbin
Jiping Qi*
Affiliation:
Department of Pathology, the First Affiliated Hospital of Harbin Medical University, Harbin
*
Department of Pathology, the First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, PR China; Email: [email protected].
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Abstract

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Background:

The objective of this study was to explore the expression of urotensin II (UII), its receptor (GPR14), and vascular endothelial growth factor (VEGF), as well as their associations in the ischaemic brains of rats with focal cerebral ischaemia, under normal and diabetic conditions.

Methods:

Diabetes mellitus (DM) was induced by injection of streptozotocin (STZ) into Sprague—Dawley rats. Focal cerebral ischaemia was induced by middle cerebral artery occlusion (MCAO) four weeks after DM onset by STZ. Rats (n=80) were divided into four groups: normal control, DM, MCAO, and DM/MCAO. Immunohistochemistry and reverse-transcriptase-polymerase chain reaction (RT-PCR) were used to detect the expression of UII, GPR14 and VEGF in the diabetic and ischaemic brain.

Results:

Expression of UII and GPR14 was increased at mRNA and protein levels in the DM and MCAO group compared with controls. In the DM/MCAO group, expression of UII and GPR14 was increased significantly in the ischaemic brain, and was accompanied by a significantly increased VEGF expression.

Conclusion:

Diabetes mellitus was seen to aggravate brain lesions after ischaemia, and UII may have an important role.

Type
Original Article
Copyright
Copyright © The Canadian Journal of Neurological 2014

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