Knockdown of LncRNA PART1 Inhibits Nerve Injury Caused by Ischemic Stroke by Regulating the Expression of miR-638

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.