Astaxanthin (ATX), which is the most abundant flavonoid in propolis, has previously shown neuroprotective properties against cerebral ischaemia‐induced apoptosis. However, the mechanisms by which ATX mediates its therapeutic effects are unclear. At present, we explored the underlying mechanisms involved in the protective effects of ATX via the phosphoinositide 3‐kinase (PI3K)/Akt/glycogen synthase kinase 3 beta (GSK3β)/nuclear factor erythroid 2‐related factor 2 (Nrf2) signalling pathway in SH‐SY5Y cells. The PI3K/Akt inhibitor LY294002 and GSK3β inhibitor LiCl were employed in this study. Pre‐treatment with ATX for 24 hours significantly decreased the oxygen and glucose deprivation (OGD)‐induced viability loss, reduced the proportion of apoptosis and regulated OGD‐mediated reactive oxygen species (ROS) production. Furthermore, ATX suppressed OGD‐caused mitochondrial membrane potential and decomposition of caspase‐3 to cleaved caspase‐3, and heightened the B‐cell lymphoma 2 (Bcl‐2)/Bax ratio. PI3K/Akt/GSK3β/Nrf2 signalling pathway activation in SH‐SY5Y cells was verified by Western blot. ATX and LiCl treatment raised the protein levels of p‐Akt, p‐GSK3β, nucleus Nrf2 and haeme oxygenase 1 (HO‐1). However, these protein expression levels decreased by treatment of LY294002. The above in vitro data indicate that ATX can confer neuroprotection against OGD‐induced apoptosis via the PI3K/Akt/GSK3β/Nrf2 signalling pathway.

中文翻译：

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虾青素通过PI3K / Akt /GSK3β/ Nrf2信号通路在体外对氧和葡萄糖剥夺损伤的神经保护作用。

虾青素（ATX）是蜂胶中含量最高的类黄酮，以前显示出对脑缺血诱导的细胞凋亡具有神经保护作用。但是，ATX介导其治疗作用的机制尚不清楚。目前，我们探讨了通过磷酸肌醇3激酶（PI3K）/ Akt /糖原合酶激酶3 beta（GSK3β）/核因子红系2相关因子2（Nrf2）信号通路参与ATX保护作用的潜在机制。 SH‐SY5Y细胞。本研究中使用了PI3K / Akt抑制剂LY294002和GSK3β抑制剂LiCl。ATX预处理24小时可显着降低氧和葡萄糖剥夺（OGD）引起的生存力丧失，减少细胞凋亡的比例并调节OGD介导的活性氧（ROS）的产生。此外，ATX抑制了OGD引起的线粒体膜电位以及caspase-3分解为caspase-3裂解，并提高了B细胞淋巴瘤2（Bcl-2）/ Bax比值。Western印迹证实了SH‐SY5Y细胞中PI3K / Akt /GSK3β/ Nrf2信号通路的激活。ATX和LiCl处理提高了p-Akt，p-GSK3β，核Nrf2和血红素加氧酶1（HO-1）的蛋白质水平。然而，通过LY294002的处理，这些蛋白质表达水平降低。上述体外数据表明，ATX可以通过PI3K / Akt /GSK3β/ Nrf2信号通路赋予神经保护，以抵抗OGD诱导的细胞凋亡。ATX和LiCl处理可提高p‐Akt，p‐GSK3β，细胞核Nrf2和血红素加氧酶1（HO-1）的蛋白质水平。然而，通过LY294002的处理，这些蛋白质表达水平降低。上述体外数据表明，ATX可以通过PI3K / Akt /GSK3β/ Nrf2信号传导通路赋予抗OGD诱导的细胞凋亡的神经保护作用。ATX和LiCl处理可提高p‐Akt，p‐GSK3β，细胞核Nrf2和血红素加氧酶1（HO-1）的蛋白质水平。然而，通过LY294002的处理，这些蛋白质表达水平降低。上述体外数据表明，ATX可以通过PI3K / Akt /GSK3β/ Nrf2信号传导通路赋予抗OGD诱导的细胞凋亡的神经保护作用。