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

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Date: July 30, 2022
Publisher: Hindawi Limited
Document Type: Article
Length: 5,039 words
Lexile Measure: 1390L

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Abstract :

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-κ B (NF-κ B) 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-κ B1, NF-κ B2, and REL mRNA. The hs-CRP results of UAP group, SAP group, and control group were 11.12±1.5mg/L, 10.23±1.3mg/L, and 4.51±1.1mg/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-κ B1, NF-κ B2, and REL mRNA were obviously higher in the SAP group compared than the indicator values in the control group (P

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Gale Document Number: GALE|A712888994