目的：明确长链非编码RNA(lncRNA)肺腺癌转移相关转录本1(MALAT1)在过氧化氢(H₂O₂)诱导的人晶状体上皮细胞系HLE-B3氧化应激与凋亡中的表达特征及调控作用。

方法：将HLE-B3细胞分为Control组与 H₂O₂组(200 μmol/L H₂O₂培养24 h)，通过流式细胞术检测活性氧簇(ROS)水平及细胞凋亡率，试剂盒测定超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性，实时荧光定量PCR检测MALAT1表达，荧光原位杂交明确其细胞定位。筛选沉默效率最佳的Si-MALAT1序列后，设置Control组、 H₂O₂组、H₂O₂+Si-NC组、H₂O₂+Si-MALAT1组，免疫荧光染色检测凋亡标志物TUNEL及Nrf2定位情况。

结果：与Control组相比， H₂O₂组细胞ROS水平显著升高，SOD、CAT活性显著降低(均P<0.001)，凋亡率升高(P<0.01)； MALAT1表达上调(P<0.01)，且定位于细胞核。沉默MALAT1后，H₂O₂诱导的细胞凋亡被显著抑制(P<0.01)。

结论：H₂O₂诱导的氧化应激可上调MALAT1表达，沉默MALAT1减轻HLE-B3细胞氧化应激损伤及凋亡，为白内障的防治提供潜在靶点。

METHODS: HLE-B3 cells were divided into Control group and H₂O₂ group(cultured with 200 μmol/L H₂O₂ for 24 h). Levels of reactive oxygen species(ROS)and cell apoptosis rates were detected by flow cytometry. Activities of superoxide dismutase(SOD)and catalase(CAT)were measured using kits, MALAT1 expression was quantified by real-time quantitative PCR, and its cellular localization was determined by fluorescence in situ hybridization. After selecting the Si-MALAT1 sequence with the highest silencing efficiency, the groups were established as Control, H₂O₂, H₂O₂+Si-NC, and H₂O₂+Si-MALAT1. Immunofluorescence staining was employed to detect the apoptosis marker TUNEL and Nrf2 nuclear translocation.

RESULTS:Compared with the Control group, the H₂O₂group exhibited significantly elevated ROS levels, markedly decreased SOD and CAT activities(both P<0.001), and a significantly increased apoptosis rate(P<0.01). MALAT1 expression was upregulated(P<0.01)and localized in the nucleus. After silencing MALAT1, H₂O₂-induced cell apoptosis was significantly inhibited(P<0.01).

CONCLUSION: H₂O₂-induced oxidative stress can increase the expression of MALAT1, and silencing MALAT1 reduces oxidative stress damage and apoptosis, providing a potential target for preventing and treating cataracts.