Increased protein and mRNA expression of endostatin in the ischemic brain tissue of rabbits after middle cerebral artery occlusion.

Heng-li Tian; Hao Chen; Yu-hui Cui; Tao XU; Liang-fu Zhou

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Increased protein and mRNA expression of endostatin in the ischemic brain tissue of rabbits after middle cerebral artery occlusion.

Author: Heng-Li TIAN ¹ ; Hao CHEN ; Yu-Hui CUI ; Tao XU ; Liang-Fu ZHOU
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1. Department of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai 200040, China.
Publication Type:Journal Article
MeSH: Animals; Brain; metabolism; physiopathology; Brain Ischemia; genetics; metabolism; physiopathology; Cerebral Arteries; metabolism; Endostatins; genetics; metabolism; Endothelium, Vascular; metabolism; Enzyme-Linked Immunosorbent Assay; Immunohistochemistry; In Situ Hybridization; Infarction, Middle Cerebral Artery; genetics; metabolism; physiopathology; Male; Neovascularization, Physiologic; physiology; Rabbits; Up-Regulation; physiology; Vascular Endothelial Growth Factor A; metabolism
From:Neuroscience Bulletin 2007;23(1):35-40
CountryChina
Language:English
Abstract:
OBJECTIVETo explore the changes of endostatin (a strong anti-angiogenesis factor) and vascular endothelial growth factor (VEGF) in the brain tissues of rabbits following cerebral ischemia induced by middle cerebral artery occlusion (MCAO).
METHODSTwenty-four New Zealand white rabbits were randomly divided into 5 groups: control (n = 5), sham-operation (n = 4), 2-hour ischemia (n = 5), 24-hour ischemia (n = 5), and 48-hour ischemia (n = 5). The expression of VEGF and endostatin were measured by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry, respectively. In situ hybridization was used to characterize the expression of mRNA for the endostatin.
RESULTSBoth the protein (at least 50%, P < 0.01) and mRNA (at least 70%, P < 0.05) of endostatin increased significantly in the ischemic brain tissues after MCAO compared with the control group. VEGF increased at least 270% in the brain after cerebral ischemia (P < 0.05).
CONCLUSIONCerebral ischemia leads to an up-regulation of endostatin in the brain, which is not associated with the increase of VEGF in the brain. The increase of endostatin may serve as a deleterious mechanism for ischemic injury through blocking angiogenesis.