Effects and mechanisms of LINC00657 on oxidative glucose deprivation-induced injury in mouse hippocampal neurons

SHI Qian; WANG Baoqi; QI Taotao; BAO Hanzhong

doi:10.7619/jcmp.20241212

Journal of Clinical Medicine in Practice > 2024 > 28(13): 82-86. > DOI: 10.7619/jcmp.20241212

SHI Qian, WANG Baoqi, QI Taotao, BAO Hanzhong. Effects and mechanisms of LINC00657 on oxidative glucose deprivation-induced injury in mouse hippocampal neurons[J]. Journal of Clinical Medicine in Practice, 2024, 28(13): 82-86. DOI: 10.7619/jcmp.20241212

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Effects and mechanisms of LINC00657 on oxidative glucose deprivation-induced injury in mouse hippocampal neurons

1.
Henan University of Traditional Chinese Medicine, Zhengzhou, Henan, 450000
2.
Department of Encephalopathy, the First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, Henan, 450000

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Received Date: March 21, 2024
Revised Date: May 15, 2024
Available Online: July 19, 2024

Graphical Abstract

Abstract

Abstract

Objective
To investigate the effects and mechanisms of LINC00657 on oxidative glucose deprivation (OGD)-induced injury in mouse hippocampal neurons.
Methods
Mouse hippocampal neuron cell line HT22 was given OGD treatment to establish an injury model, with normally cultured HT22 cells as controls. The si-NC, si-LINC00657, microRNA(miR)-NC, and miR-224-3p mimics were transfected into HT22 cells, followed by OGD treatment. Co-transfection of si-LINC00657 and anti-miR-NC, or co-transfection of si-LINC00657 and anti-miR-224-3p, was performed in HT22 cells before OGD treatment. Real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect the relative expression levels of LINC00657 and miR-224-3p. CCK-8 assay and flow cytometry were used to detect cell viability and apoptosis rate, respectively. Kits were used to detect the activities of lactate dehydrogenase (LDH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and the level of malondialdehyde (MDA). Dual-luciferase reporter gene assay was used to detect the effect of miR-224-3p overexpression on the luciferase activity of wild-type LINC00657 vector (WT-LINC00657) and mutant LINC00657 vector (MUT-LINC00657).
Results
Compared with controls, the expression of LINC00657 was upregulated and the expression of miR-224-3p was downregulated in OGD-induced HT22 cells (P < 0.05). Compared with transfection of si-NC or miR-NC, transfection of si-LINC00657 or miR-224-3p mimics resulted in increased cell viability, SOD activity, and GSH-Px activity, as well as decreased apoptosis rate, LDH activity, and MDA level(P < 0.05). Overexpression of miR-224-3p reduced the luciferase activity of WT-LINC00657 (P < 0.05). Compared with cells co-transfected with si-LINC00657 and anti-miR-NC, cells co-transfected with si-LINC00657 and anti-miR-224-3p showed decreased cell viability, increased apoptosis rate, increased LDH activity and MDA level, and decreased SOD and GSH-Px activities (P < 0.05).
Conclusion
Interference with LINC00657 can promote cell proliferation, inhibit apoptosis and oxidative stress response by upregulating miR-224-3p, thereby alleviating OGD-induced injury in mouse hippocampal neurons.
- hippocampal neurons,
- oxidative glucose deprivation,
- LINC00657,
- microRNA-224-3p,
- cell proliferation,
- apoptosis,
- oxidative stress

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References (15)

References

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Effects and mechanisms of LINC00657 on oxidative glucose deprivation-induced injury in mouse hippocampal neurons