The International journal of neuroscience · 2026
The predictive value of serum CXCL2 and CXCL8 levels for early neurological deterioration in patients with penetrating artery disease-type ischaemic stroke.
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Zhong Yi, Liu Bei
Аннотация
OBJECTIVE: To evaluate whether serum C-X-C motif chemokine ligand 2 (CXCL2) and C-X-C motif chemokine ligand 8 (CXCL8) predict early neurological deterioration (END) in penetrating artery disease (PAD)-type ischaemic stroke.
METHODS: This retrospective study included 146 PAD patients (June 2022-October 2024). Patients were stratified into END (n = 22) and non-END (n = 124) groups. Bioinformatics analysis using the GEO database and protein-protein interaction (PPI) analysis were performed. Serum CXCL2 and CXCL8 levels were measured by enzyme-linked immunosorbent assay (ELISA). Pearson correlation, receiver operating characteristic (ROC) curve, and logistic regression analyses were performed, followed by nomogram construction.
RESULTS: Bioinformatics analysis revealed CXCL2 and CXCL8 upregulation in cerebral infarction. END patients were older, had prolonged onset-to-admission times, higher admission National Institutes of Health Stroke Scale scores, and a higher branch atheromatous disease prevalence (all p < 0.05). END patients had elevated serum CXCL2 and CXCL8 levels (p < 0.05), which were positively correlated (r = 0.202, p = 0.015). ROC analysis indicated that the combination of CXCL2 and CXCL8 produced an area under the curve of 0.799 (95% CI: 0.720-0.878), outperforming individual markers. LASSO regression identified age, CXCL2, and CXCL8 as key variables. Multivariate analysis revealed age (OR = 1.140, 95% CI: 1.053-1.235, p = 0.001), CXCL2 (OR = 1.024, 95% CI: 1.006-1.043, p = 0.008), and CXCL8 (OR = 1.009, 95% CI: 1.003-1.016, p = 0.003) as independent END risk factors. The nomogram demonstrated excellent discrimination (training: 0.874; validation: 0.856) and good calibration (Hosmer-Lemeshow p > 0.05).
CONCLUSIONS: Serum CXCL2 and CXCL8 demonstrate potential as biomarkers for identifying END in acute PAD.
METHODS: This retrospective study included 146 PAD patients (June 2022-October 2024). Patients were stratified into END (n = 22) and non-END (n = 124) groups. Bioinformatics analysis using the GEO database and protein-protein interaction (PPI) analysis were performed. Serum CXCL2 and CXCL8 levels were measured by enzyme-linked immunosorbent assay (ELISA). Pearson correlation, receiver operating characteristic (ROC) curve, and logistic regression analyses were performed, followed by nomogram construction.
RESULTS: Bioinformatics analysis revealed CXCL2 and CXCL8 upregulation in cerebral infarction. END patients were older, had prolonged onset-to-admission times, higher admission National Institutes of Health Stroke Scale scores, and a higher branch atheromatous disease prevalence (all p < 0.05). END patients had elevated serum CXCL2 and CXCL8 levels (p < 0.05), which were positively correlated (r = 0.202, p = 0.015). ROC analysis indicated that the combination of CXCL2 and CXCL8 produced an area under the curve of 0.799 (95% CI: 0.720-0.878), outperforming individual markers. LASSO regression identified age, CXCL2, and CXCL8 as key variables. Multivariate analysis revealed age (OR = 1.140, 95% CI: 1.053-1.235, p = 0.001), CXCL2 (OR = 1.024, 95% CI: 1.006-1.043, p = 0.008), and CXCL8 (OR = 1.009, 95% CI: 1.003-1.016, p = 0.003) as independent END risk factors. The nomogram demonstrated excellent discrimination (training: 0.874; validation: 0.856) and good calibration (Hosmer-Lemeshow p > 0.05).
CONCLUSIONS: Serum CXCL2 and CXCL8 demonstrate potential as biomarkers for identifying END in acute PAD.