IMR Press / JIN / Volume 22 / Issue 2 / DOI: 10.31083/j.jin2202033
Open Access Original Research
Quantitative Proteomics Reveals Neuroprotective Mechanism of Ginkgolide B in Aβ1-42-induced N2a Neuroblastoma Cells
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1 Department of Geriatrics, The Second Hospital of Hebei Medical University, 050000 Shijiazhuang, Hebei, China
*Correspondence: (Guofeng Yang)
J. Integr. Neurosci. 2023, 22(2), 33;
Submitted: 7 August 2022 | Revised: 5 September 2022 | Accepted: 6 September 2022 | Published: 14 February 2023
Copyright: © 2023 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

Objective: Ginkgolide B (GB) possesses anti-inflammatory, antioxidant, and anti-apoptotic properties against neurotoxicity induced by amyloid beta (Aβ), but the potential neuroprotective effects of GB in Alzheimer’s therapies remain elusive. We aimed to conduct proteomic analysis of Aβ1-42 induced cell injury with GB pretreatment to uncover the underlying pharmacological mechanisms of GB. Methods: Tandem mass tag (TMT) labeled liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was applied to analyze protein expression in Aβ1-42 induced mouse neuroblastoma N2a cells with or without GB pretreatment. Proteins with fold change >1.5 and p < 0.1 from two independent experiments were regarded as differentially expressed proteins (DEPs). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to analyze the functional annotation information of DEPs. Two key proteins osteopontin (SPP1) and ferritin heavy chain 1 (FTH1) were validated in another three samples using western blot and quantitative real-time PCR. Results: We identified a total of 61 DEPs in GB treated N2a cells, including 42 upregulated and 19 downregulated proteins. Bioinformatic analysis showed that DEPs mainly participated in the regulation of cell death and ferroptosis by down-regulating SPP1 protein and up-regulating FTH1 protein. Conclusions: Our findings demonstrate that GB treatment provides neuroprotective effects on Aβ1-42 induced cell injury, which may be related to the regulation of cell death and ferroptosis. The research puts forward new insights into the potential protein targets of GB in the treatment of Alzheimer’s disease (AD).

Alzheimer's disease
Ginkgolide B
tandem mass tag
bioinformatics analysis
cell death
2020172/Scientific Research Project of Hebei Administration of Traditional Chinese Medicine
Fig. 1.
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