葡萄糖限制对丙烯醛诱导的永生化小鼠海马神经元神经毒性的保护作用OA

[Objective]to evaluate the effects and underlying mechanisms of a glucose restriction(GR)regimen on acrolein-induced neurotoxicity and AD-related pathology.[Methods]Immortalized mouse hippocampal HT22 cells were pretreated with culture media containing different glucose concentrations(25 mmol/L,17.5 mmol/L,and 12.5 mmol/L),followed by incubation with 25 μmol/L acrolein for specified durations.Cell viability and apoptosis were assessed using MTT assay and flow cytometry,respectively.Changes in glutathione(GSH),superoxide dismutase(SOD),and malondialdehyde(MDA)levels were measured using enzyme linked immunosorbent assay(ELISA)kits.Alterations in the expression of BDNF/TrkB signaling proteins and key enzymes involved in amyloid precursor protein(APP)metabolism were evaluated by Western blot.[Results]Pretreatment with GR significantly attenuated acrolein-induced loss of cell viability in HT22 cells.GR also alleviated the depletion of GSH and SOD,reduced MDA levels,and thereby ameliorated acrolein-induced oxidative damage(P＜0.05).Furthermore,GR inhibited acrolein-triggered early apoptosis.Notably,the GR regimen protectively modulated the expression of BDNF/TrkB signaling pathway components and key APP-metabolizing enzymes(ADAM10 and BACE1)(P＜0.05).[Conclusion]GR exerts neuroprotective effects against acrolein-induced toxicity,suggesting its potential in preventing or delaying the development of AD.