title: Ginkgolides protect primary cortical neurons from potassium cyanide-induced hypoxic injury.
abstract: In this study, we investigated the effects of ginkgolides (Gins A, B, C and J), the main constituent of the non-flavone fraction of EGb 761, on hypoxic injury induced by potassium cyanide (KCN) in primary cortical neurons. The neurons were pretreated with or without ginkgolides for 24 h before incubation with KCN for 4 h. Cell viability was then determined by a MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyletrazolium bromide] assay and lactate dehydrogenase (LDH) release from neurons into the medium was measured. The morphological changes of neurons were observed under inverse microscopy and electron microscopy. The results demonstrated that KCN (0.05 mmol/l) significantly decreased cell viability and increased LDH release (P < 0.05 versus the control). The characteristic changes of neuronal morphology induced by KCN were observed. However, pretreatment of neurons with 37.5 microg/ml of ginkgolides (ginkgolides + KCN group) led to a significant increase in cell viability, a decrease in LDH release (P < 0.05 versus the KCN group) and a remarkable improvement in cellular morphology in hypoxic neurons compared with the KCN group. The data suggested that ginkgolides have a significant role to protect the primary cortical neurons from hypoxic injury induced by KCN.
authors.affiliation: Institute for Nautical Medicine and Key Laboratory of Neuroregeneration, Nantong University, Nantong, 226001, People's Republic of China. zhulili65@yahoo.com
authors.forename: Li
authors.initials: L
authors.lastname: Zhu
authors.forename: You Jia
authors.initials: YJ
authors.lastname: Xu
authors.forename: Fang
authors.initials: F
authors.lastname: Du
authors.forename: Zhong Ming
authors.initials: ZM
authors.lastname: Qian
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D046934:Ginkgolides / Q000494:pharmacology* / Q000627:therapeutic use; D002534:Hypoxia, Brain / Q000139:chemically induced / Q000517:prevention & control*; D007202:Indicators and Reagents; D007770:L-Lactate Dehydrogenase / Q000032:analysis / Q000378:metabolism; D051379:Mice; D008813:Mice, Inbred ICR; D009410:Nerve Degeneration / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D011042:Poisons / Q000633:toxicity; D011190:Potassium Cyanide / Q000037:antagonists & inhibitors / Q000633:toxicity; D013778:Tetrazolium Salts; D016896:Treatment Outcome
chemical_list: D046934:Ginkgolides; D007202:Indicators and Reagents; D018696:Neuroprotective Agents; D011042:Poisons; D013778:Tetrazolium Salts; D007770:L-Lactate Dehydrogenase; D011190:Potassium Cyanide