2010Acta Academiae Medicinae Qingdao UniversitatisRequires access

EXPRESSION OF VASCULAR ENDOTHELIAL GROWTH FACTOR IN A RAT MODEL OF CEREBRAL ISCHEMIA TOLERANCE

G Wang

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Abstract

Objective To investigate the expression of vascular endothelial growth factor (VEGF) at different time points after reperfusion in a cerebral ischemia-tolerant rat model induced by focal ischemia preconditioning, and study the significance of VEGF in cerebral ischemia tolerance.MethodsFifty-five healthy Wistar rats were randomized to three groups: the sham operation group (SS+SS,n=5), the sham opertation and subsequent middle cerebral artery occlusion (MCAO) group (SS+MCAO,n=25), and the ischemia preconditioning and subsequent MCAO group (IP+MCAO,n=25). The latter two groups were further divided into five subgroups. For ischemia preconditioning, the rats were performed MCAO with filament ligation for 10 min. On the 1st, 3rd, 7th, 14th and 21st day after ischemia preconditioning, the rats were given the second MCAO for 2 h followed by 22 h reperfusion. Brain tissues were biopsied and tissue sections stained with hematoxylin and eosin (HE) for histological study and determination of infarction volume. The models were evaluated with neurological deficit score. The expression of VEGF was determined by immunohistochemical staining. ResultsCompared with the corresponding subgroups of SS+MCAO group, the neurologic scores were significantly reduced, the volume of cerebral infarction was significantly decreased and the expression of VEGF significantly increased in the 1st-, 3rd-and 7st-day subgroups of IP+MCAO group (t=2.357-11.479,P0.05). ConclusionIschemia preconditioning induced cerebral ischemia tolerance. IP-induced up-regulation of VEGF expression plays an important role in the induction of ischemia tolerance.

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Objective To investigate the expression of vascular endothelial growth factor (VEGF) at different time points after reperfusion in a cerebral ischemia-tolerant rat model induced by focal ischemia preconditioning, and study the significance of VEGF in cerebral ischemia tolerance.MethodsFifty-five healthy Wistar rats were randomized to three groups: the sham operation group (SS+SS,n=5), the sham opertation and subsequent middle cerebral artery occlusion (MCAO) group (SS+MCAO,n=25), and the ischemia preconditioning and subsequent MCAO group (IP+MCAO,n=25). The latter two groups were further divided into five subgroups. For ischemia preconditioning, the rats were performed MCAO with filament ligation for 10 min. On the 1st, 3rd, 7th, 14th and 21st day after ischemia preconditioning, the rats were given the second MCAO for 2 h followed by 22 h reperfusion. Brain tissues were biopsied and tissue sections stained with hematoxylin and eosin (HE) for histological study and determination of infarction volume. The models were evaluated with neurological deficit score. The expression of VEGF was determined by immunohistochemical staining. ResultsCompared with the corresponding subgroups of SS+MCAO group, the neurologic scores were significantly reduced, the volume of cerebral infarction was significantly decreased and the expression of VEGF significantly increased in the 1st-, 3rd-and 7st-day subgroups of IP+MCAO group (t=2.357-11.479,P0.05). ConclusionIschemia preconditioning induced cerebral ischemia tolerance. IP-induced up-regulation of VEGF expression plays an important role in the induction of ischemia tolerance.

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Available abstract

Objective To investigate the expression of vascular endothelial growth factor (VEGF) at different time points after reperfusion in a cerebral ischemia-tolerant rat model induced by focal ischemia preconditioning, and study the significance of VEGF in cerebral ischemia tolerance.MethodsFifty-five healthy Wistar rats were randomized to three groups: the sham operation group (SS+SS,n=5), the sham opertation and subsequent middle cerebral artery occlusion (MCAO) group (SS+MCAO,n=25), and the ischemia preconditioning and subsequent MCAO group (IP+MCAO,n=25). The latter two groups were further divided into five subgroups. For ischemia preconditioning, the rats were performed MCAO with filament ligation for 10 min. On the 1st, 3rd, 7th, 14th and 21st day after ischemia preconditioning, the rats were given the second MCAO for 2 h followed by 22 h reperfusion. Brain tissues were biopsied and tissue sections stained with hematoxylin and eosin (HE) for histological study and determination of infarction volume. The models were evaluated with neurological deficit score. The expression of VEGF was determined by immunohistochemical staining. ResultsCompared with the corresponding subgroups of SS+MCAO group, the neurologic scores were significantly reduced, the volume of cerebral infarction was significantly decreased and the expression of VEGF significantly increased in the 1st-, 3rd-and 7st-day subgroups of IP+MCAO group (t=2.357-11.479,P0.05). ConclusionIschemia preconditioning induced cerebral ischemia tolerance. IP-induced up-regulation of VEGF expression plays an important role in the induction of ischemia tolerance.

Key concepts: Ischemia, Medicine, H&E stain, Vascular endothelial growth factor, Immunohistochemistry, Ligation, Infarction, Anesthesia

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EXPRESSION OF VASCULAR ENDOTHELIAL GROWTH FACTOR IN A RAT MODEL OF CEREBRAL ISCHEMIA TOLERANCE — Research Paper | ScholarLens