Urinary Trypsin Inhibitor Reduced Inflammation Response Induced by Hyperlipidemia

Area of Science:

• Cardiovascular Research
• Inflammation Biology
• Molecular Medicine

Background:

• Atherosclerosis is a chronic inflammatory disease.
• Hyperlipidemia is a key risk factor, driving inflammatory responses.
• Urinary trypsin inhibitor (UTI) is investigated for its anti-inflammatory potential.

Purpose of the Study:

• To investigate the role of UTI in hyperlipidemia-induced inflammation.
• To assess UTI's effect on neointimal hyperplasia in a rabbit model.
• To explore the impact of UTI on microRNA-181b (miR-181b) expression.

Main Methods:

• Rabbits with induced iliac artery injury were divided into control, model, and UTI groups.
• Histological analysis measured neointimal thickness (NT) and neointimal to media ratio (N/M).
• Evaluated blood lipids, inflammatory factors (IL-6, TNF-α), macrophage infiltration, and miR-181b expression.

Main Results:

• UTI therapy reduced serum inflammatory factors and macrophage infiltration in the iliac artery.
• Hyperlipidemia decreased miR-181b expression and increased NT and N/M ratio.
• UTI administration restored miR-181b levels and inhibited neointimal formation.

Conclusions:

• Urinary trypsin inhibitor mitigates neointimal hyperplasia by suppressing hyperlipidemia-induced inflammation.
• UTI demonstrates potential as an anti-atherosclerosis supplement.
• The study highlights the link between miR-181b, inflammation, and neointimal formation.