Exploring the role of cytochrome P450 family 1 subfamily B member 1 and quercetin in modulating neuropathic pain after spinal cord injury.

Spinal cord injury (SCI) represents a notable global health challenge, with neuropathic pain (NP) being a common complication that intensifies patient suffering. Existing research tends to overlook the temporal aspects of NP and fails to offer targeted treatment options. To tackle this issue, the present study initially examined genome‑wide association study summaries related to NP, incorporating expression quantitative trait locus (eQTL) from blood samples through summary‑based Mendelian randomization. This allowed the investigation of the association between NP and eQTL, facilitating the identification of genes linked to the risk of NP. Following this, weighted gene co‑expression network analysis of a Gene Expression Omnibus dataset was utilized to identify SCI‑related module genes, resulting in the detection of 218 shared genes across these analyses. Subsequent functional enrichment assessments, protein‑protein interaction evaluations and machine learning technique analyses, including least absolute shrinkage and selection operator regression, random forest and support vector machine recursive feature elimination analyses, highlighted three central genes: Glycerol‑3‑phosphate dehydrogenase 1‑like, epoxide hydrolase 2 and cytochrome P450 family 1 subfamily B member 1 (CYP1B1). Additionally, network pharmacology and molecular docking analyses confirmed CYP1B1 as a viable therapeutic target. A analysis of single‑cell RNA sequencing datasets demonstrated an increase in CYP1B1 expression within spinal cord fibroblasts following SCI. Furthermore, quercetin (Que) was shown to inhibit CYP1B1 expression and reduce NP (based on mechanical paw withdrawal threshold and thermal paw withdrawal latency) in murine models. The results of the present study highlight the important role of spinal cord fibroblast CYP1B1 as a notable contributor to NP following SCI and suggest that Que may serve as a promising mechanism‑based therapeutic option.