This study attempted to determine the effect of EphA2 on H₂O₂-treated lens epithelial cells (SRA01/04) and the underlying mechanisms. MTT assay and flow cytometry were performed to assess cell viability and cell apoptosis. Western blot was carried out to examine the levels of proteins associated with apoptosis and autophagy. Our results revealed that EphA2 significantly elevated the reduced cell viability, and inhibited the increased cell apoptosis in H₂O₂-treated SRA01/04 cells, along with the significant up-regulated Bcl-2 and down-regulated Cleaved-caspase-3 and Bax protein levels, but which were all abolished by Rapa (autophagy activator). We also found that EphA2 significantly suppressed cell autophagy in H₂O₂-treated SRA01/04 cells. Additionally, EphA2 significantly up-regulated the protein levels of p-Akt and p-mTOR in H₂O₂-treated SRA01/04 cells, and the inhibition of Akt by MK-2206 and inhibition of mTOR by Rapa both obviously reversed EphA2-mediated the inhibition of autophagy in H₂O₂-treated SRA01/04 cells. In summary, these data demonstrated that EphA2 inhibited the apoptosis of SRA01/04 cells by inhibiting autophagy via activating PI3K/Akt/mTOR pathway.

该研究试图确定 EphA2 对 H ₂ O ₂处理的晶状体上皮细胞 (SRA01/04) 的影响及其潜在机制。进行MTT测定和流式细胞术以评估细胞活力和细胞凋亡。进行蛋白质印迹以检查与细胞凋亡和自噬相关的蛋白质水平。我们的结果表明，EphA2 显着提高了降低的细胞活力，并抑制了 H ₂ O ₂处理的 SRA01/04 细胞中增加的细胞凋亡，以及显着上调的 Bcl-2 和下调的 Cleaved-caspase-3 和Bax 蛋白水平，但都被 Rapa（自噬激活剂）消除了。我们还发现 EphA2 显着抑制了 H _{2 中的}细胞自噬O ₂处理的SRA01/04细胞。此外，EphA2显着上调H ₂ O ₂处理的SRA01/04细胞中p-Akt和p-mTOR的蛋白水平，MK-2206对Akt的抑制和Rapa对mTOR的抑制均明显逆转了EphA2-在H ₂ O ₂处理的SRA01/04细胞中介导自噬的抑制。总之，这些数据表明EphA2通过激活PI3K/Akt/mTOR通路抑制自噬来抑制SRA01/04细胞的凋亡。