Abstract: Objective: To analyze the protective effects of vitamin B5 and vitamin B12 on a Parkinson’s disease model of SH-SY5Y cells. Methods: SH-SY5Y cells were induced using 1-methyl-4-phenylpyridinium (MPP+) to establish the model. SH-SY5Y cells in the logarithmic growth phase were divided into five groups: a normal control group, a model group (treated with 2 mmol/L MPP+ for 24 h), a VB5 group (sequentially treated with 5 μmol/L VB5 for 4 h followed by 2 mmol/L MPP+ for 24 h), a VB12 group (sequentially treated with 10 μmol/L VB12 for 4 h followed by 2 mmol/L MPP+ for 24 h), and a VB5 + VB12 group (sequentially treated with 5 μmol/L VB5 + 50 μmol/L VB12 for 4 h followed by 2 mmol/L MPP+ for 24 h). Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay, apoptosis was measured by flow cytometry using Annexin V-FITC/PI, intracellular reactive oxygen species (ROS) levels were quantified using the 2’,7’-dichlorodihydrofluorescein diacetate (DCFH-DA) fluorescent probe, mitochondrial membrane potential was evaluated with the JC-1 fluorescent probe, ATP levels were determined by the phosphomolybdate colorimetric method, and the protein and mRNA expression of Bip, CCAAT/enhancer-binding protein-homologous protein (CHOP), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cytochrome c (Cyt-c), and caspase-3 were detected by Western blot and real-time polymerase chain reaction (PCR). Results: Compared with the normal control group, cell viability was significantly reduced in the model group, apoptosis was significantly increased, mitochondrial membrane potential and ATP content were significantly decreased, and ROS levels were elevated. Additionally, the expression levels of the pro-apoptotic proteins Bax and caspase-3 were significantly up-regulated, while the expression of the anti-apoptotic protein Bcl-2 was significantly down-regulated in the model group. The expression levels of the endoplasmic reticulum stress-related proteins Bip, CHOP, protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor 2α (eIF2α), and activating transcription factor 4 (ATF4), as well as Cyt-c, were significantly increased in the model group. Compared with the model group, both the VB5 and VB12 groups partially reversed these changes, and the combined use of VB5 and VB12 showed a more pronounced effect than either treatment alone. Conclusion: VB5 and VB12 can alleviate MPP+-induced Parkinson’s disease injury in SH-SY5Y cells, and the mechanism may be related to the regulation of the Bip-PERK-eIF2α-CHOP signaling pathway and the improvement of mitochondrial dysfunction by VB5 and VB12.

Key words: VB5; VB12; SH-SY5Y cells; 1-methyl-4-phenylpyridinium-induced Parkinson’s disease model; endoplasmic reticulum stress; mitochondrial function