The aim of this study was to investigate whether the neuroprotective effects of astragaloside IV (AS-IV) against hydrogen peroxide (H2O2)-induced damage on human neuroblastoma cell line (SH-SY5Y) are associated with synaptic plasticity. The concentration screening of AS-IV and H2O2 on SH-SY5Y cells and the protective effects of AS-IV on SH-SY5Y cells under H2O2 stress were all determined by MTT assay. The expression of postsynaptic density 95 (PSD-95) and growth-associated protein 43 (GAP-43) were measured by western blot (WB) and inmunofluorescence staining assay under the same treatment conditions. According to the MTT results, the concentration of H2O2 at 50 μmol/L for 3 h was used for the cell damage model, and various concentrations of AS-IV (0.1, 0.2, 0.3, and 0.4 μmol/L) were used to affect SH-SY5Y cells. The MTT results showed that pretreatment of SH-SY5Y cells with AS-IV (0.1, 0.2, 0.3, and 0.4 μmol/L) attenuated the damage induced by H2O2 (50 μmol/L, 51.62% cell viability) and increased cell viability to 64.19, 63.48, 65.86, and 65.81%, respectively. Western blot analysis and immunofluorescence staining showed that the protective effects of AS-IV against SH-SY5Y cell damage caused by H2O2 resulted in reduced expression of PSD-95 and increased expression of GAP-43 in comparison with the H2O2 treatment group. The conclusion shows that AS-IV protected SH-SY5Y cells and enhanced their viability under H2O2 stress. AS-IV may facilitate presynaptic and postsynaptic plasticity to exert protective effects against oxidative damage of SH-SY5Y cells.

中文翻译：

---

黄芪甲苷对 SH-SY5Y 细胞 H2O2 诱导损伤的神经保护作用与突触可塑性有关

本研究的目的是研究黄芪甲苷 (AS-IV) 对过氧化氢 (H2O2) 诱导的人神经母细胞瘤细胞系 (SH-SY5Y) 损伤的神经保护作用是否与突触可塑性有关。AS-IV和H2O2对SH-SY5Y细胞的浓度筛选以及AS-IV对H2O2胁迫下SH-SY5Y细胞的保护作用均采用MTT法测定。在相同处理条件下，通过蛋白质印迹 (WB) 和免疫荧光染色测定法测量突触后密度 95 (PSD-95) 和生长相关蛋白 43 (GAP-43) 的表达。根据MTT结果，细胞损伤模型采用50 μmol/L H2O2浓度3 h，不同浓度AS-IV（0.1、0.2、0.3和0.4 μmol/L）影响SH-SY5Y 细胞。MTT结果显示，用AS-IV（0.1、0.2、0.3和0.4 μmol/L）预处理SH-SY5Y细胞减弱了H2O2诱导的损伤（50 μmol/L，51.62%的细胞活力）并增加了细胞活力分别为 64.19、63.48、65.86 和 65.81%。Western印迹分析和免疫荧光染色表明，与H2O2处理组相比，AS-IV对H2O2引起的SH-SY5Y细胞损伤的保护作用导致PSD-95表达降低和GAP-43表达增加。结论表明 AS-IV 保护了 SH-SY5Y 细胞并增强了它们在 H2O2 胁迫下的活力。AS-IV 可以促进突触前和突触后的可塑性，发挥对 SH-SY5Y 细胞氧化损伤的保护作用。4 μmol/L) 减弱了 H2O2 诱导的损伤（50 μmol/L，细胞活力 51.62%），将细胞活力分别提高到 64.19、63.48、65.86 和 65.81%。Western印迹分析和免疫荧光染色表明，与H2O2处理组相比，AS-IV对H2O2引起的SH-SY5Y细胞损伤的保护作用导致PSD-95表达降低和GAP-43表达增加。结论表明 AS-IV 保护了 SH-SY5Y 细胞并增强了它们在 H2O2 胁迫下的活力。AS-IV 可以促进突触前和突触后的可塑性，发挥对 SH-SY5Y 细胞氧化损伤的保护作用。4 μmol/L) 减弱了 H2O2 诱导的损伤（50 μmol/L，细胞活力 51.62%），将细胞活力分别提高到 64.19、63.48、65.86 和 65.81%。Western印迹分析和免疫荧光染色表明，与H2O2处理组相比，AS-IV对H2O2引起的SH-SY5Y细胞损伤的保护作用导致PSD-95表达降低和GAP-43表达增加。结论表明 AS-IV 保护了 SH-SY5Y 细胞并增强了它们在 H2O2 胁迫下的活力。AS-IV 可以促进突触前和突触后的可塑性，发挥对 SH-SY5Y 细胞氧化损伤的保护作用。Western印迹分析和免疫荧光染色表明，与H2O2处理组相比，AS-IV对H2O2引起的SH-SY5Y细胞损伤的保护作用导致PSD-95表达降低和GAP-43表达增加。结论表明 AS-IV 保护了 SH-SY5Y 细胞并增强了它们在 H2O2 胁迫下的活力。AS-IV 可以促进突触前和突触后的可塑性，发挥对 SH-SY5Y 细胞氧化损伤的保护作用。Western印迹分析和免疫荧光染色表明，与H2O2处理组相比，AS-IV对H2O2引起的SH-SY5Y细胞损伤的保护作用导致PSD-95表达降低和GAP-43表达增加。结论表明 AS-IV 保护了 SH-SY5Y 细胞并增强了它们在 H2O2 胁迫下的活力。AS-IV 可以促进突触前和突触后的可塑性，发挥对 SH-SY5Y 细胞氧化损伤的保护作用。