Ying Deng1, Junying Kong2. 1. Department of Emergency, Second Affiliated Hospital of Harbin Medical University, Harbin, Hei Long Jiang, China. 2. Department of Emergency, Second Affiliated Hospital of Harbin Medical University, Harbin, Hei Long Jiang, China kjygtg123@163.com.
Abstract
INTRODUCTION AND OBJECTIVES: Atherosclerosis is recognized as a chronic inflammatory disease. The aim of this study was to examine the role of urinary trypsin inhibitor (UTI) in inflammation response induced by hyperlipidemia in rabbits. METHODS: Thirty rabbits after injury of the right iliac artery endothelium were randomly divided into 3 groups: control group, model group, and UTI group. Iliac arteries were isolated and histology was performed on arterial regions that were injured by balloon after 8 weeks. Neointimal thickness (NT) and neointimal to media radio (N/M) were measured. Blood lipids, interleukin 6, and tumor necrosis factor-α were evaluated. Macrophages were evaluated by immunohistochemical analysis. MicroRNA-181b (miR-181b) was measured by reverse transcriptase-polymerase chain reaction. RESULTS: Urinary trypsin inhibitor therapy decreased serum inflammatory factor levels without significant changes in blood lipids. Compared with model group, UTI reduced macrophage infiltration of iliac artery (13.91 ± 2.03% vs 24.21 ± 8.94%, P < .01). Hyperlipidemia reduced the expression of miR-181b and increased NT and N/M ratio. Systemic administration of UTI rescued miR-181b expression and inhibited neointimal formation. CONCLUSIONS: Urinary trypsin inhibitor could reduce neointimal hyperplasia by inhibiting inflammatory response induced by hyperlipidemia and may become a potential antiatherosclerosis supplement.
INTRODUCTION AND OBJECTIVES:Atherosclerosis is recognized as a chronic inflammatory disease. The aim of this study was to examine the role of urinary trypsin inhibitor (UTI) in inflammation response induced by hyperlipidemia in rabbits. METHODS: Thirty rabbits after injury of the right iliac artery endothelium were randomly divided into 3 groups: control group, model group, and UTI group. Iliac arteries were isolated and histology was performed on arterial regions that were injured by balloon after 8 weeks. Neointimal thickness (NT) and neointimal to media radio (N/M) were measured. Blood lipids, interleukin 6, and tumor necrosis factor-α were evaluated. Macrophages were evaluated by immunohistochemical analysis. MicroRNA-181b (miR-181b) was measured by reverse transcriptase-polymerase chain reaction. RESULTS: Urinary trypsin inhibitor therapy decreased serum inflammatory factor levels without significant changes in blood lipids. Compared with model group, UTI reduced macrophage infiltration of iliac artery (13.91 ± 2.03% vs 24.21 ± 8.94%, P < .01). Hyperlipidemia reduced the expression of miR-181b and increased NT and N/M ratio. Systemic administration of UTI rescued miR-181b expression and inhibited neointimal formation. CONCLUSIONS: Urinary trypsin inhibitor could reduce neointimal hyperplasia by inhibiting inflammatory response induced by hyperlipidemia and may become a potential antiatherosclerosis supplement.