2006Journal of Apoplexy and Nervous DiseasesRequires access

NO upgrades expression of VEGF protein and mRNA in local ischemic brain tissues of rabbits

Cui Yu-hui

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Abstract

Objective No and VEGF may mediate angiogenesis and interact to promote angiogenesis in an ischemic brain. The aim of the study as to investigate the effects of exogenous NO on VEGF expression. Methods NO donor,L-arginine was intravenously administered to rabbits daily after cerebral ischemia. The expression of VEGF protein was assessed by ELISA. Flurosecent RT-PCR was carried out to estimate the mRNA levels of VEGF. Brain edema was determined by measuring brain water content. Results Compared to control groups,L-arginine significantly enhanced VEGF protein levels(1.180±0.433ng/ml vs 0.649±0.274ng/ml,P 0.05 ) and VEGF mRNA expression(0.3402±8.876×10~ -3 vs 0.2025±0.0413,P 0.05 ) in ischemic brain tissue,and diminished water levels of ischemic brain tissue. Conclusion The findings that exogenous NO enhances VEGF expression of ischemic brain tissue and alleviates brain edema suggest combination treatment with NO donor and VEGF may have synergistic effects on neuroprotection after cerebral ischemia.

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Objective No and VEGF may mediate angiogenesis and interact to promote angiogenesis in an ischemic brain. The aim of the study as to investigate the effects of exogenous NO on VEGF expression. Methods NO donor,L-arginine was intravenously administered to rabbits daily after cerebral ischemia. The expression of VEGF protein was assessed by ELISA. Flurosecent RT-PCR was carried out to estimate the mRNA levels of VEGF. Brain edema was determined by measuring brain water content. Results Compared to control groups,L-arginine significantly enhanced VEGF protein levels(1.180±0.433ng/ml vs 0.649±0.274ng/ml,P 0.05 ) and VEGF mRNA expression(0.3402±8.876×10~ -3 vs 0.2025±0.0413,P 0.05 ) in ischemic brain tissue,and diminished water levels of ischemic brain tissue. Conclusion The findings that exogenous NO enhances VEGF expression of ischemic brain tissue and alleviates brain edema suggest combination treatment with NO donor and VEGF may have synergistic effects on neuroprotection after cerebral ischemia.

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Available abstract

Objective No and VEGF may mediate angiogenesis and interact to promote angiogenesis in an ischemic brain. The aim of the study as to investigate the effects of exogenous NO on VEGF expression. Methods NO donor,L-arginine was intravenously administered to rabbits daily after cerebral ischemia. The expression of VEGF protein was assessed by ELISA. Flurosecent RT-PCR was carried out to estimate the mRNA levels of VEGF. Brain edema was determined by measuring brain water content. Results Compared to control groups,L-arginine significantly enhanced VEGF protein levels(1.180±0.433ng/ml vs 0.649±0.274ng/ml,P 0.05 ) and VEGF mRNA expression(0.3402±8.876×10~ -3 vs 0.2025±0.0413,P 0.05 ) in ischemic brain tissue,and diminished water levels of ischemic brain tissue. Conclusion The findings that exogenous NO enhances VEGF expression of ischemic brain tissue and alleviates brain edema suggest combination treatment with NO donor and VEGF may have synergistic effects on neuroprotection after cerebral ischemia.

Key concepts: Neuroprotection, VEGF receptors, Messenger RNA, Ischemia, Angiogenesis, Brain tissue, Brain edema, Vascular endothelial growth factor

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