Here, (-)-Tetrahydroalstonine (THA) was isolated from Alstonia scholaris and investigated for its neuroprotective effect towards oxygen-glucose deprivation/re-oxygenation (OGD/R)-induced neuronal damage. In this study, primary cortical neurons were pre-treated with THA and then subjected to OGD/R induction. The cell viability was tested by the MTT assay, and the states of the autophagy-lysosomal pathway and Akt/mTOR pathway were monitored by Western blot analysis. The findings suggested that THA administration increased the cell viability of OGD/R-induced cortical neurons. Autophagic activity and lysosomal dysfunction were found at the early stage of OGD/R, which were significantly ameliorated by THA treatment. Meanwhile, the protective effect of THA was significantly reversed by the lysosome inhibitor. Additionally, THA significantly activated the Akt/mTOR pathway, which was suppressed after OGD/R induction. In summary, THA exhibited promising protective effects against OGD/R-induced neuronal injury by autophagy regulation through the Akt/mTOR pathway.

中文翻译：

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(-)-Tetrahydroalstonine 通过自噬调节对 OGD/R 诱导的神经元损伤的保护作用。

在这里，从 Alstonia schorisis 中分离出 (-)-Tetrahydroalstonine (THA)，并研究其对氧-葡萄糖剥夺/再氧合 (OGD/R) 诱导的神经元损伤的神经保护作用。在这项研究中，初级皮层神经元用 THA 预处理，然后进行 OGD/R 诱导。MTT法检测细胞活力，Western blot分析监测自噬-溶酶体通路和Akt/mTOR通路的状态。研究结果表明，THA 给药增加了 OGD/R 诱导的皮质神经元的细胞活力。在 OGD/R 的早期发现自噬活性和溶酶体功能障碍，通过 THA 治疗显着改善。同时，THA 的保护作用被溶酶体抑制剂显着逆转。此外，THA 显着激活 Akt/mTOR 通路，该通路在 OGD/R 诱导后被抑制。总之，THA 通过 Akt/mTOR 通路的自噬调节对 OGD/R 诱导的神经元损伤表现出良好的保护作用。