目的：探究LncRNA MIRLET7BHG对人神经母细胞瘤细胞系（SH-SY5Y）在缺血再灌注损伤中的作
用。方法：采用氧糖剥夺/复氧（oxygen and glucose deprivation/reoxygenation，OGD/R）模型模拟体外
SH-SY5Y细胞缺血再灌注损伤，并通过RT-qPCR检查LncRNA MIRLET7BHG的水平。构建SH-SY5Y 细
胞LncRNA MIRLET7BHG敲低模型，利用MTT、流式细胞术和蛋白质印迹法评估常规培养或OGD/R处理
后细胞的活力和凋亡水平。结果：OGD/R处理后，SH-SY5Y细胞凋亡率显著升高，细胞存活率均显著下降，
氧化应激标志物的水平均显著升高，LncRNA MIRLET7BHG转录水平显著上升。敲低SH-SY5Y细胞中的
LncRNA MIRLET7BHG，降低了常规培养或OGD/R处理的SH-SY5Y的活力，促进了细胞凋亡。结论：Ln
cRNA MIRLET7BHG 对 OGD/R 诱导的 SH-SY5Y 细胞凋亡中有一定的抑制作用，LncRNA MIRLET7BHG
转录水平上调，提示可能存在某种负反馈机制。
To investigate the role of LncRNA MIRLET7BHG in human neuroblastoma cell line
(SH-SY5Y) during ischemia reperfusion injury. Methods: An oxygen and glucose deprivation/reoxygenation
(OGD/R) model was used to simulate in vitro ischemia reperfusion injury in SH-SY5Y cells, and the level of
LncRNA MIRLET7BHG was examined by RT-qPCR. A LncRNA MIRLET7BHG knockdown model of
SH-SY5Y cells was constructed, and MTT, flow cytometry, and Western blotting were used to evaluate the
viability and apoptosis levels of cells after normal culture or OGD/R treatment. Results: After OGD/R
treatment, the apoptosis rate of SH-SY5Y cells increased significantly, the cell survival rate decreased
significantly, the levels of oxidative stress markers increased significantly, and the transcription level of LncRNA
MIRLET7BHG increased significantly. Knocking down LncRNA MIRLET7BHG in SH-SY5Y cells reduced the
viability of SH-SY5Y cells under normal culture or OGD/R treatment and promoted cell apoptosis.
Conclusion: LncRNA MIRLET7BHG has a certain inhibitory effect on OGD/R-induced apoptosis of
SH-SY5Y cells. The up-regulation of LncRNA MIRLET7BHG transcription level suggests that there may be a
negative feedback mechanism.
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