Abstract 

Background: 

Human neutrophil peptide-1(HNP-1) is a commonly investigated therapeutic agent. However, its role in hypertensive left ventricular hypertrophy(HLVH) remains unclear. 

Methods:

We measured HNP-1 levels in patients with hypertension and treated HLVH rat and H9c2 cell hypertrophy models with HNP-1. Cardiomyocyte hypertrophy indexes (i.e., single-cell surface area, left ventricle fibro area, BNP levels, and β-MHC levels) were measured using hematoxylin-eosin and Masson’s trichrome staining and WB. NF-кB signaling factors (i.e., IKKβ, p-IKKβ, IкBα, p-IкBα, p65, and p-p 65) were measured by WB and qPCR. Lastly, inflammatory factors (i.e., IL-6, IL-1α, and TNF-α) were measured by ELISA.

Results: HNP-1 levels were lower in the exposure vs. control groups (M (95% CI), 48.83 (45.64–52.26) vs. 59.03 (55.62–62.54), p = 0.000). A decrease in HNP-1 was associated with HLVH occurrence in patients. HLVH rat and H9c2 cell hypertrophy models revealed elevated cardiomyocyte hypertrophy indexes and NF-кB signaling and inflammatory factors. However, each HNP-1 treatment group experienced a decline in the aforementioned indices as compared with the model groups. 

Conclusion: 

HNP-1 decrease is a risk factor for HLVH. HNP-1 treatment may reverse HLVH by inhibiting NF-кB signal pathways.