Astaxanthin （ATX） , the most abundant flavonoids in propolis, has been proven to exert neuroprotective property against cerebral ischemia-induced apoptosis. However, the mechanisms by which ATX mediates its thera- peutic effects in vitro are unclear. In the present study, the article explored the underlying mechanisms involved in the protective effects of ATX via the PI3IC/Akt/GSK3β/Nrf2 signaling pathway in SH-SY5Y cells. For study of mechanism, the phosphoinositide 3 kinase （PI3K）-Akt inhibitor LY294002, Glycogen synthase kinase 3β （GSK313） inhibitor LiC1 were used. Pre-treatmentwith ATX for 24h significantly reduced the OGD induced viability loss, apoptotic rate and attenuated OGD-mediated ROS production. In addition, ATX inhibited OGD-induced mito- chondrial membrane potential, decreased Bcl-2/Bax ratio. PI3 IC/Akt/GSK3β/Nrf2 signaling pathway activation in SH-SY5Y was tested by Western blot. Nrf2 expression was increasing by ATX and counteracted by PI3IC/Akt in- hibitor LY294002, GSK3β inhibitor LiC1 in SH-SY5Y. Nrf2 Immunocytochemistry showed Nrf2 nuclear transloca- tion was increasing by ATX and counteracted by LY294002 or LiC1 in SH-SY5Y, respectively. It may be suggested that astaxanthin against cerebral ischemia-induced apoptosis in vitro via a programmed PI3 IC/Akt/GSK3β/Nrf2 sig- naling pathway in vitro.
