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Antagonistic effects of extract from leaves of Ginkgo biloba on glutamate neurotoxicity

ZHU, L ; WU, J ; LIAO, H ; GAO, J ; ZHAO, X.-N ; ZHANG, Z.-X

Zhōngguó yàolĭ xuébào, 1997-07, Vol.18 (4), p.344-347

Beijing: Science Press

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Título:
Antagonistic effects of extract from leaves of Ginkgo biloba on glutamate neurotoxicity
Autor: ZHU, L ; WU, J ; LIAO, H ; GAO, J ; ZHAO, X.-N ; ZHANG, Z.-X
Assuntos: Animals ; Arcuate Nucleus of Hypothalamus - drug effects ; Arcuate Nucleus of Hypothalamus - metabolism ; Biological and medical sciences ; Calcium - metabolism ; Cells, Cultured ; Cerebral Cortex - cytology ; Diterpenes ; Fetus ; General pharmacology ; Ginkgo biloba ; Ginkgolides ; Glutamic Acid ; Lactones - pharmacology ; Medical sciences ; Mice ; Pharmacognosy. Homeopathy. Health food ; Pharmacology. Drug treatments ; Plant Extracts - pharmacology ; Plant Leaves ; Plants, Medicinal
É parte de: Zhōngguó yàolĭ xuébào, 1997-07, Vol.18 (4), p.344-347
Descrição: To determine whether the extract of leaves of Ginkgo biloba L (EGb) and several active constituents of EGb have protective effects against glutamate (Glu)-induced neuronal damage. Microscopy and image analysis of nucleus areas in the arcuate nuclei (AN) of mice were made. The neuronal viability in primary cultures from mouse cerebral cortex was assessed using MTT [3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide] staining and the intracellular free calcium concentration ([Ca2+]i) of single neuron was measured using Fura-2. EGb (2.5 mg.L-1) and its constituent ginkgolide B (Gin B, 2 mg.L-1) protected the neuronal viability against Glu-induced injury, and prevented the Glu-induced elevation in [Ca2+]i. EGb (3-10 mg.kg-1) attenuated the decrease of nucleus areas in arcuate nuclei induced by Glu (1 g.kg-1, s.c.). EGb and Gin B prevent neurons from Glu neurotoxicity through reduction of the rise in [Ca2+]i.
Editor: Beijing: Science Press
Idioma: Inglês

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Antagonistic effects of extract from leaves of Ginkgo biloba on glutamate neurotoxicity

ZHU, L ; WU, J ; LIAO, H ; GAO, J ; ZHAO, X.-N ; ZHANG, Z.-X

Beijing: Science Press

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