Silencing SOX2-OT alleviates A <b>β</b> -induced damage to neurons and microglial cells by targeting miR-143-3p in Alzheimer’s disease

This research focuses on examining the function of the long non-coding RNA SOX2-OT in Alzheimer's disease (AD) and its interaction with the microRNA miR-143-3p, revealing their functions in neurons and microglial cells and their effects on AD-related pathology. SOX2-OT and miR-143-3p levels were detected through qRT-PCR of serum from AD patients and SH-SY5Y and HMC3 cells treated with Aβ_25-35. The online databases LncBook, DIANA, and LncACTdb 3.0 were utilized to predict the targeting relationship between SOX2-OT and miR-143-3p. We performed dual-luciferase reporter assays to confirm their interaction. Additionally, MTT assays and flow cytometry were used to assess the impact of the SOX2-OT/miR-143-3p axis on the fate of Aβ_25-35-treated SH-SY5Y and HMC3 cells. ELISA was employed to measure the concentrations of oxidative stress and inflammatory factors. SOX2-OT levels were significantly elevated in AD patients serum and SH-SY5Y and HMC3 cells, while miR-143-3p levels were significantly reduced. SOX2-OT targeted to miR-143-3p. Silencing SOX2-OT significantly alleviated the reduction in cell proliferation and the increase in apoptosis caused by Aβ, reducing oxidative stress and the release of inflammatory factors. In contrast, inhibition of miR-143-3p reversed these effects. In conclusion, the SOX2-OT/miR-143-3p axis influences AD-related pathological states by regulating cell proliferation, apoptosis, neuroinflammation, and oxidative stress.