Background
Ginkgolide K is a terpene trilactone that has been found in G. biloba and has diverse biological activities.1,2,3 It reduces corpus callosum demyelination, increases the distance traveled in the elevated plus maze, and reduces immobility time in the forced swim test in mice in a model of cuprizone-induced demyelination when administered at a dose of 20 mg/kg per day.2 Ginkgolide K (4 and 8 mg/kg) reduces infarct volume, improves neurological deficits, reverses decreases in superoxide dismutase (SOD) activity, and reverses increases in the levels of malondialdehyde (MDA) and nitric oxide (NO) in cerebral ischemic sections and serum in a rat model of cerebral ischemia-reperfusion injury induced by middle cerebral artery occlusion (MCAO).3
1.van Beek, T.A.Ginkgolides and bilobalide: Their physical, chromatographic and spectroscopic propertiesBioorg. Med. Chem.13(17)5001-5012(2005)
2.Li, Q.-Y., Miao, Q., Sui, R.-X., et al.Ginkgolide K supports remyelination via induction of astrocytic IGF/PI3K/Nrf2 axisInt. Immunopharmacol.75105819(2019)
3.Ma, S., Yin, H., Chen, L., et al.Neuroprotective effect of ginkgolide K against acute ischemic stroke on middle cerebral ischemia occlusion in ratsJ. Nat. Med.66(1)25-31(2012)
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