The intrinsic mechanism
of postherpetic neuralgia (PHN) remains
unclear. Herein, we aimed to seek the hub proteins in the cerebrospinal
fluid (CSF), which display significant changes between the PHN and
nonpainful patients (Control). First, the proteomic results showed
that compared with the Control-CSF, there were 100 upregulated and
50 downregulated differentially expressed proteins (DEPs) in the PHN-CSF.
Besides, functional analyses including gene ontology (GO), Kyoto Encyclopedia
of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA)
revealed that biological processes and pathways including complement
activation, infection, coagulation, and lipid metabolism were activated,
while synaptic organization was suppressed. Next, the protein–protein
interaction (PPI) analysis indicated that increased PLG, F2, APOA1,
APOA2, SERPINC1, and KNG1 and reduced APOE, which were all enriched
in the top pathways according to the KEGG analysis, were defined as
hub proteins. Finally, three of the hub proteins, such as PLG, APOA1,
and APOE, were reconfirmed in a larger cohort using both enzyme-linked
immunosorbent assay (ELISA) and Western blotting methods. Above all,
the results indicated that PLG, APOA1, and APOE and their involved
processes such as infection, inflammation, cholesterol metabolism,
and coagulation shall be potential therapeutic approaches. (The raw
mass spectrometry proteome data and search results have been deposited
to the iProx-integrated Proteome Resources () with the data
set identifier IPX0007372000.)