Granzyme B as a potential biological target in toxic encephalopathy: A big data-based exploratory analysis

Area of Science:

• Neuroscience
• Immunology
• Genomics

Background:

• Toxic encephalopathy is a central nervous system disorder resulting from toxic substances.
• Granzyme B (GZMB) is a serine protease involved in immune regulation and disease progression.
• The specific role of GZMB in toxic encephalopathy pathogenesis is not well understood.

Purpose of the Study:

• To explore the association between Granzyme B (GZMB) and toxic encephalopathy using big data analysis.
• To identify potential biomarkers and therapeutic targets for toxic encephalopathy.

Main Methods:

• Utilized the toxic encephalopathy dataset GSE253309 from the Gene Expression Omnibus database.
• Identified differentially expressed genes using the "limma" R package.
• Performed Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses.
• Constructed a protein-protein interaction network using the STRING database and identified hub genes with Cytoscape.

Main Results:

• Identified 994 differentially expressed genes, with GZMB moderately overexpressed in toxic encephalopathy tissues (log2 fold change = 0.70, P = 0.00087).
• GZMB and related genes were enriched in pathways including TGF-beta signaling and apoptosis, implicated in immune regulation and neuronal injury.
• Protein-protein interaction network analysis confirmed GZMB as a key hub gene.

Conclusions:

• Elevated GZMB expression is implicated in the pathogenesis and progression of toxic encephalopathy.
• GZMB represents a potential disease biomarker and therapeutic target for toxic encephalopathy.
• Compounds like β-escin sodium and methylprednisolone may modulate GZMB expression to alleviate neuronal damage.