Study on the Expression of Synaptic Vesicle Proteins and the Improvement of Inflammatory Injury in Human Neuroblastoma Cells SH-SY5Y by Lactobacillus rhamnosus B6 Metabolic Products of Fermented Skim Milk

This study investigated the effects of Lacticaseibacillus rhamnosus B6 metabolic products of fermented skim milk (LB6S) on synaptic vesicle proteins (Syp) in human neuroblastoma SH-SY5Y cells and their protective mechanism against lipopolysaccharide (LPS)-induced neuroinflammatory injury. The viability of SH-SY5Y cells was assessed via the CCK-8 assay to determine the optimal concentration of LB6S. The reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting (WB) were employed to analyze Syp expression. An LPS-induced neuroinflammatory model was established to evaluate LB6S-mediated regulation of pro-inflammatory cytokines, apoptotic factors and signaling pathways through RT-qPCR and WB. The results indicated that LB6S exhibited no cytotoxicity at concentrations up to 500 μg/mL (P>0.05). At 500 μg/mL, LB6S significantly upregulated transcriptional expression of the synapse-related genes Sirt1, Syp, Vamp2, and Vglut1 (P<0.05) and increased Syp levels (P<0.05). In LPS-damaged cells, 500 μg/mL LB6S downregulated the pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 (P<0.05). Mechanistically, LB6S inhibited neuroinflammation by modulating mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) pathways, reducing pro-apoptotic Bax and increasing anti-apoptotic Bcl-2 expression (P<0.05). In conclusion, LB6S regulates synaptic proteins, promotes Syp expression, and ameliorates neuroinflammatory injury by modulating apoptotic and inflammatory mediators through MAPK/NF-κB signaling.