Experimental analysis shows knockdown of lncRNA PART1 improves cell viability in ischemic stroke, indicating potential therapeutic value.
Ischemic stroke (IS), a life‐threatening disease, carries a high risk of disability and death. Reverse transcription quantitative real‐time polymerase chain reaction was utilized to measure the PART1 and miR‐638 expression in patients with IS and oxygen–glucose deprivation/reoxygenation (OGD/R) model. Superoxide dismutase (SOD), malondialdehyde (MDA), lactate dehydrogenase (LDH), interleukin‐6 (IL‐6) and tumor necrosis factor‐α (TNF‐α) levels were determined by enzyme‐linked immunosorbent assay kit. Cell viability was assessed using the cell counting kit‐8 assay. Apoptotic cells were analyzed by flow cytometry. To explore the interaction between PART1 and miR‐638, luciferase reporter and RNA immunoprecipitation (RIP) assays were carried out. In patients with IS and OGD/R‐treated cells, PART1 exhibited upregulation, whereas miR‐638 showed downregulation; there was a negative correlation between these two molecules. Knockdown of PART1 increased cell viability, decreased apoptosis, lowered MDA, LDH, IL‐6 and TNF‐α levels, and increased SOD activity. PART1 negatively regulated miR‐638 expression, and inhibition of miR‐638 reduced the protective effect of the knockdown of PART1 on OGD/R‐treated cells. This study demonstrated that knockdown of PART1 inhibits IS‐induced neurological injury by regulating miR‐638 expression, which promotes the understanding of IS disease and provides new options for the treatment of the disease.
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Xu et al. (2025) studied this question.
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