Intraventricular vascular endothelial growth factor antibody increases infarct volume following transient cerebral ischemia
Abstract
AIM:
To clarify the role of vascular endothelial growth factor (VEGF) in neuronal damage induced by cerebral ischemia.
METHODS:
Expression of VEGF in adult rat brain was measured by immunohistochemistry. Transient middle cerebral artery occlusion (MCAO) model was induced by placing a nylon thread in the lumen of the internal carotid artery. The infarct volume was shown with 2,3,5-triphenyltetrazolium chloride (TTC) staining and quantitated by computer image analyzer with and without VEGF antibody treatment.
RESULTS:
VEGF expression was widely distributed in neuronal cells besides vascular endothelial cells, and the neuronal distribution of VEGF was specific. After intraventricular treatment with VEGF antibody (0.1 g.L-1 daily, for 7 d following the ischemia), infarct volume in the antibody treatment was increased versus vehicle-treated rats [(21.6 +/- 2.7 vs 16 +/- 6) mm3, P < 0.05] respectively.
CONCLUSION:
Intraventricular injection of VEGF antibody increased the infarct volume after focal cerebral ischemia in rats, suggesting that expression of neuronal VEGF may be one of neuronal protective mechanisms.
Keywords:
To clarify the role of vascular endothelial growth factor (VEGF) in neuronal damage induced by cerebral ischemia.
METHODS:
Expression of VEGF in adult rat brain was measured by immunohistochemistry. Transient middle cerebral artery occlusion (MCAO) model was induced by placing a nylon thread in the lumen of the internal carotid artery. The infarct volume was shown with 2,3,5-triphenyltetrazolium chloride (TTC) staining and quantitated by computer image analyzer with and without VEGF antibody treatment.
RESULTS:
VEGF expression was widely distributed in neuronal cells besides vascular endothelial cells, and the neuronal distribution of VEGF was specific. After intraventricular treatment with VEGF antibody (0.1 g.L-1 daily, for 7 d following the ischemia), infarct volume in the antibody treatment was increased versus vehicle-treated rats [(21.6 +/- 2.7 vs 16 +/- 6) mm3, P < 0.05] respectively.
CONCLUSION:
Intraventricular injection of VEGF antibody increased the infarct volume after focal cerebral ischemia in rats, suggesting that expression of neuronal VEGF may be one of neuronal protective mechanisms.