Circulating brain-derived neurotrophic factor dysregulation and its linkage with lipid level, stenosis degree, and inflammatory cytokines in coronary heart disease

Background Brain-derived neurotrophic factor (BDNF) regulates the lipid metabolism, atherosclerosis plaque formation, and inflammatory process, while the study about its clinical role in coronary heart disease (CHD) is few. The present study intended to explore the expression of BDNF and its relationship with stenosis, inflammation, and adhesion molecules in CHD patients. Methods After serum samples were obtained from 207 CHD patients, BDNF, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, IL-6, IL-8, IL-17A, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) levels were determined using ELISA. Then, the BDNF level was also examined in 40 disease controls (DCs) and 40 healthy controls (HCs), separately. Results BDNF was lower in CHD patients than in DCs and HCs (median (95% confidential interval) value: 5.6 (3.5-9.6) ng/mL vs. 10.7 (6.1-17.0) ng/mL and 12.6 (9.4-18.2) ng/mL, both p < 0.001). BDNF could well distinguish CHD patients from DCs (area under the curve [AUC]: 0.739) and HCs (AUC: 0.857). BDNF was negatively associated with triglyceride (p = 0.014), total cholesterol (p = 0.037), and low-density lipoprotein cholesterol (p = 0.008). BDNF was negatively associated with CRP (p < 0.001), TNF-alpha (p < 0.001), IL-1 beta (p = 0.008), and IL-8 (p < 0.001). BDNF was negatively related to VCAM-1 (p < 0.001) and ICAM-1 (p = 0.003). BDNF was negatively linked with the Gensini score (p < 0.001). Conclusion BDNF reflects the lipid dysregulation, inflammatory status, and stenosis degree in CHD patients.

Automated summary

The study found that BDNF levels were lower in CHD patients compared to disease controls and healthy controls, and were negatively correlated with triglyceride, total cholesterol, low-density lipoprotein cholesterol, CRP, TNF-alpha, IL-1 beta, IL-8, VCAM-1, ICAM-1, and Gensini score.