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  • Title: [Neuroprotective effect of exogenous vascular endothelial growth factor on anoxic rat spinal cord astrocyte and the underlying mechanism].
    Author: Jiang S, Ding XM, Mao BY.
    Journal: Sichuan Da Xue Xue Bao Yi Xue Ban; 2005 Nov; 36(6):792-6. PubMed ID: 16334555.
    Abstract:
    OBJECTIVE: To observe the effect of hypoxia on primary cultured rat spinal cord astrocyte and investigate the neuroprotective effect of exogenous vascular endothelial growth factor (VEGF) on anoxic astrocyte in vitro. METHODS: The rat embryonic spinal cord astrocytes were cultured and identified by cellular morphology and glial fibrillary acidic protein (GFAP). The astrocytes were treated with VEGF at different concentrations (10 ng/ml-100 ng/ml) as well as with VEGF receptor (Flk-1) inhibitor SU1498. Then the astrocytes were exposed to hypoxia for different time. The light microscope, MTT assay, TUNEL labeling and SABC immuno-histochemistry were used to measure and observe the changes of the astrocytes in cell morphology, growth, proliferation, GFAP identified that 98% of the purified 1-week cultured cells apoptosis, VEGF and Flk-1 expression. RESULTS: were astrocytes. 8-12 hours hypoxia obviously induced the activity of astrocyte. The cytobody became bigger, the cytoskeleton grew thicker. The activity of proliferation decreased but apoptosis index increased. The GFAP, VEGF and Flk-1 expression increased. The treatment with 50 ng/ml VEGF 20-24 hours before hypoxia apparently enhanced the activity, decreased the apoptosis index of the astrocytes, and hence improved the hypoxia-injuried astrocytes. Howerver, 700 ng/ml SU1498 obviously inhibited the neuroprotective effect of VEGF on anoxic astrocytes. CONCLUSION: Hypoxia induces reactive activity of astrocyte. The exogenous VEGF exerts neuroprotective effect on astrocytes via VEGF receptor-Flk-1.
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