caa a22 4500 445377259 CHVBK 20180317143006.0 cr unu---uuuuu 170323e20110801xx s 000 0 eng 10.1007/s00702-011-0637-2 doi (NATIONALLICENCE)springer-10.1007/s00702-011-0637-2 Ginkgo extract EGb 761® shields from slowly accumulating neurodegenerative-like changes in a newly developed cell culture model induced by the combined action of low doses of antimycin A1 and 2-deoxy- d -glucose [Elektronische Daten] [Konstanze Plaschke, Marion Bergmann, Jürgen Kopitz] Different cell culture models were already used to analyze the molecular base of the neuroprotective activities of the Ginkgo biloba extract EGb 761® after a single or short-term application. In these previous studies cells were severely injured with agents that promptly induce fatal cellular damage, like vast oxidative stress or mitochondrial dysfunction, and the protective effects of EGb 761® on such acute damage were evaluated. Our present study aimed to test EGb 761® action in cell cultures, where cellular functions are only moderately impaired by a longer lasting, but relatively modest oxidative stress, reduction of mitochondrial function and reduced intracellular energy levels, thereby causing only slow occurence of cellular damage over a time period of 2weeks. To this end we used neuroblastoma cells (SK-N-MC) that were treated with low doses of a combination of antimycin A1 and 2-deoxy-d-glucose. Addition of EGb 761® to the culture medium efficiently shielded the cells from progressing injury by reduced ATP-levels, oxidized redox state, lipid peroxidation damage and oxidative damage of mitochondrial DNA. As a result the cells were protected from apoptotic death that was observed in cultures without EGb 761® after 2weeks of damage occurence. This cell culture system characterizing moderate cellular stress will be applied in future studies to further investigate the mode of action of single EGb 761® compounds. Springer-Verlag, 2011 Aging nationallicence Ginkgo biloba nationallicence Mitochondria nationallicence Neurodegeneration nationallicence Neuroprotection nationallicence Oxidative stress nationallicence Plaschke Konstanze Clinic of Anaesthesiology, University Hospital of Heidelberg, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany aut Bergmann Marion Institute of Pathology, University Hospital of Heidelberg, Im Neuenheimer Feld 220, 69120, Heidelberg, Germany aut Kopitz Jürgen Institute of Pathology, University Hospital of Heidelberg, Im Neuenheimer Feld 220, 69120, Heidelberg, Germany aut Journal of Neural Transmission Springer Vienna 118/8(2011-08-01), 1247-1254 0300-9564 118:8<1247 2011 118 702 https://doi.org/10.1007/s00702-011-0637-2 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00702-011-0637-2 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Plaschke Konstanze Clinic of Anaesthesiology, University Hospital of Heidelberg, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany aut NATIONALLICENCE 700 1- Bergmann Marion Institute of Pathology, University Hospital of Heidelberg, Im Neuenheimer Feld 220, 69120, Heidelberg, Germany aut NATIONALLICENCE 700 1- Kopitz Jürgen Institute of Pathology, University Hospital of Heidelberg, Im Neuenheimer Feld 220, 69120, Heidelberg, Germany aut NATIONALLICENCE 773 0- Journal of Neural Transmission Springer Vienna 118/8(2011-08-01), 1247-1254 0300-9564 118:8<1247 2011 118 702 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer