The Mechanism of Inflammatory Factors and Soluble Vascular Cell Adhesion Molecule-1 Regulated by Nuclear Transcription Factor NF-κB in Unstable Angina Pectoris

This work is aimed at exploring the mechanism of inflammatory factors and soluble vascular cell adhesion molecule-1 (sVCAM-1) regulated by nuclear transcription factor-κB (NF-κB) in unstable angina pectoris (UAP). 60 patients with unstable angina pectoris (UAP), 60 patients with stable angina pectoris (SAP), and some healthy people (controls) were selected and included. Peripheral venous blood (PVB) of all subjects was collected to detect blood routine. The enzyme-linked immunosorbent assay (ELISA) was adopted for detecting Visfatin, sVCAM-1, soluble intervascular cell adhesion molecule-1 (sICAM-1), and inflammatory factors; flow cytometry (FCM) was to detect the CD63 and CD62P; real-time fluorescence quantitative polymerase chain reaction (rt-qPCR) was employed to detect the NF-κB1, NF-κB2, and REL mRNA. The hs-CRP results of UAP group, SAP group, and control group were 11.12 ± 1.5 mg/L, 10.23 ± 1.3 mg/L, and 4.51 ± 1.1 mg/L, respectively. The CD62P results of UAP group, SAP group, and control group were 16.07 ± 2.5%, 11.09 ± 1.8%, and 22.15 ± 0.4%, respectively. The high-sensitivity C-reactive protein (hs-CRP), inflammatory factors (IL-6, IL-17, IL-23, IL-1β, and tumor necrosis factor α (TNF-α)), CD63, CD62P, NF-κB1, NF-κB2, and REL mRNA were obviously higher in the SAP group compared than the indicator values in the control group (P < 0.05). The relative REL expression results of UAP group, SAP group, and control group were 3.77 ± 1.5, 2.2 ± 0.6, and 1 ± 0.4, respectively. The inflammatory factors, Visfatin, sVCAM-1, sICAM-1, CD63, CD62P, NF-κB1, NF-κB2, and REL mRNA in the UAP group showed higher levels in contrast to the other two groups (P < 0.05). In summary, UAP patients had marked activation of the IL-23/IL-17 inflammatory axis, high expressions of sVCAM-1 and sICAM-1, and activation of the NF-κB pathway. Increase of inflammatory factors and sVCAM-1 regulated by NF-κB was closely correlated with UAP.