目的：观察芒果苷对过氧化氢（H2O2）诱导SH-SY5Y细胞建立帕金森病细胞模型的细胞损伤的保护 作用，并探讨其作用的分子机制。方法：培养SH-SY5Y细胞，分为空白对照组（PBS平行处理）、模型组（含 100 μmol/L 的 H2O2培养基处理细胞 4 h）、芒果苷高、中、低剂量组（先用含芒果苷 100 nmol/L、50 nmol/L、 25 nmol/L的培养基处理4 h后，加入200 μmol/L的H2O2培养基处理细胞4 h）。采用MTT法检测芒果苷对 损伤的 SH-SY5Y 细胞活力的影响；western-blot 检测 SH-SY5Y 细胞中 DUSP6、ERK1/2、Keap1、Nrf2 和 HO-1蛋白的表达水平；试剂盒检测培养基中乳酸脱氢酶（LDH）水平、细胞内丙二醛（MDA）和超氧化物歧 化酶（SOD）水平。结果：与空白对照组相比，模型组细胞存活率显著降低，LDH和MDA水平升高，SOD水 平降低。与模型组比较，芒果苷高、中、低剂量组细胞存活率显著升高，LDH和MDA水平降低，SOD水平升 高。与空白对照组相比，模型组中的DUSP6蛋白表达增加，p-ERK1/2蛋白表达减少；与模型组比较，芒果 苷高、中、低剂量组DUSP6蛋白表达减少，p-ERK1/2蛋白表达增加。与空白对照组相比，模型组中的Nrf2 和HO-1蛋白表达减少，Keap1蛋白表达增多；与模型组比较，芒果苷高、中、低剂量组Nrf2和HO-1蛋白表达 增多，Keap1蛋白表达减少。结论：芒果苷对H2O2诱导的SH-SY5Y细胞损伤具有显著的保护作用，其机制 可能与芒果苷调控DUSP6/ERK1/2与Keap1/Nrf2通路，改善氧化应激相关。

To investigate the neuroprotective effect and mechanism of mangiferin on SH-SY5Y cell injury induced by H2O2 in the cellular model of Parkinson’s disease. Methods: SH-SY5Y cells were divided into the control group, model group, and high, medium, and low dose mangiferin groups. The cells were incubated with PBS in the control group, with 100 μmol/L H2O2 for 4 h in the model group, and pretreated with mangiferin (25, 50, and 100 nmol/L) for 4 h then incubated with 200 μmol/L H2O2 for 4 h in the high, medium, and low dose mangiferin groups. The MTT assay was used to detect the survival rate and Western-blot to detect the expression levels of DUSP6 and ERK1/2 in SH-SY5Y cells. Reagent test kits were used to measure the level of lactate dehydrogenase (LDH) in the medium and the level of malondialdehyde (MDA) and superoxide dismutase (SOD) in the cells. Results: Compared with the control group，the model group showed a significantly decreased cell survival rate, increased LDA and MDA levels, and decreased SOD levels. Compared with the model group, the high, medium, and low dose mangiferin groups showed significantly increased cell survival rates, decreased LDH and MDA levels, and increased SOD levels. Compared with the control group, the model group displayed increased DUSP6 expression and decreased p-ERK1/2 expression. Compared with the model group, the high, medium, and low dose mangiferin groups displayed decreased DUSP6 expression and increased p-ERK1/2 expression. The expression of Nrf2 and HO-1 was reduced and that of Keap1 increased in the model group compared to the control group. The expression of Nrf2 and HO-1 was increased and that of Keap1 reduced in the high, medium, and low dose mangiferin groups compared to the model group. Conclusion: Mangiferin confers a significant protective effect against the injury induced by H2O2 in SH-SY5Y cells, and the mechanism may be related to the inhibition of oxidative stress via the DUSP6/ERK1/2 and Keap1/Nrf2 pathway.