The effect of miR‑155‑5p on long‑term memory of sleep‑deprived mice through the BDNF/NF‑κB pathway

Sleep deprivation (SD) is a prevalent sleep issue in modern society that significantly impairs neurological function and quality of life in affected individuals. This study seeks to investigate the involvement of the miR‑155‑5p/BDNF axis in SD mice, aiming to establish a theoretical foundation for potential treatment strategies. Male C57BL/6 mice were utilized in the construction of a SD model using the flower pot technique. HT22 cells were selected for cellular experiments. The Morris water maze was employed to assess the learning and memory capabilities of the mice. HE staining was utilized to observe pathological changes in hippocampal tissue. Levels of IL‑1β, IL‑6, and TNF‑α were analyzed using ELISA. The expression level of miR‑155‑5p was quantified via RT‑qPCR. The binding between miR‑155‑5p and brain‑derived neurotrophic factor (BDNF) was confirmed through a dual‑luciferase reporter assay. Apoptosis of hippocampal neurons was assessed using TUNEL. Western blot analysis was conducted to evaluate the expression levels of BDNF, p65, and p‑p65. The Morris water maze test revealed that the mice exhibited prolonged escape latency, decreased swimming velocity, and reduced time spent in the target platform quadrant, which are indicative of a successful construction of the SD model. The observed cognitive deficits in the mice were associated with SD‑induced damage to the hippocampal tissue, leading to increased levels of miR‑155‑5p and decreased levels of BDNF. miR‑155‑5p was found to directly bind to BDNF, thereby suppressing its mRNA and protein expression. The upregulation of BDNF effectively mitigated hippocampal damage by attenuating cell apoptosis and reducing inflammation levels in SD mice. Additionally, the BDNF/NF‑κB pathway was found to be suppressed in SD mice through the downregulation of miR‑155‑5p. Therefore, the silencing of miR‑155‑5p inhibited the activation of the NF‑κB pathway by upregulating BDNF, which improved long‑term memory and reduced neuronal damage in SD mice.