OBJECTIVES: The aims of this study were to evaluate the effect of urinary trypsin inhibitor (UTI) on the regulation of inflammatory cytokines induced by lipopolysaccharide (LPS) and the reduction of neointimal formation in rabbits. METHODS AND RESULTS: Rabbits subjected to iliac artery balloon injury were randomly divided into three groups: control group (balloon injury), LPS group (LPS + balloon injury) and UTI group (UTI + LPS + balloon injury). Systemic markers of inflammation (serum IL-1β and TNF-α levels measured by ELISA) were increased after LPS administration. Arterial nuclear factor-κB (NF-κB/p65) at 28 days after injury was 31.50 ± 7.08 % of total cells in controls and 73.50 ± 6.90 % in LPS group (P < 0.05). Morphometric analysis of the injured arteries at 28 days revealed significantly increased luminal stenosis (45.81 ± 5.31 vs 27.93 ± 2.85 %, P < 0.05) and neointima-to-media ratio (1.40 ± 0.15 vs 0.68 ± 0.12, P < 0.05) in LPS-treated animals compared with controls. This effect was reduced by UTI administration. Serum IL-1β and TNF-α levels and NF-κB/p65 expression were significantly increased in correlation with the severity of intimal hyperplasia and inhibited by UTI. CONCLUSIONS: Systemic inflammatory response concurrently with arterial vascular injury facilitated neointimal formation. UTI reduced neointimal hyperplasia by regulating inflammatory response and could be considered as a potential anti-restenosis supplement.
OBJECTIVES: The aims of this study were to evaluate the effect of urinary trypsin inhibitor (UTI) on the regulation of inflammatory cytokines induced by lipopolysaccharide (LPS) and the reduction of neointimal formation in rabbits. METHODS AND RESULTS:Rabbits subjected to iliac artery balloon injury were randomly divided into three groups: control group (balloon injury), LPS group (LPS + balloon injury) and UTI group (UTI + LPS + balloon injury). Systemic markers of inflammation (serum IL-1β and TNF-α levels measured by ELISA) were increased after LPS administration. Arterial nuclear factor-κB (NF-κB/p65) at 28 days after injury was 31.50 ± 7.08 % of total cells in controls and 73.50 ± 6.90 % in LPS group (P < 0.05). Morphometric analysis of the injured arteries at 28 days revealed significantly increased luminal stenosis (45.81 ± 5.31 vs 27.93 ± 2.85 %, P < 0.05) and neointima-to-media ratio (1.40 ± 0.15 vs 0.68 ± 0.12, P < 0.05) in LPS-treated animals compared with controls. This effect was reduced by UTI administration. Serum IL-1β and TNF-α levels and NF-κB/p65 expression were significantly increased in correlation with the severity of intimal hyperplasia and inhibited by UTI. CONCLUSIONS: Systemic inflammatory response concurrently with arterial vascular injury facilitated neointimal formation. UTI reduced neointimal hyperplasia by regulating inflammatory response and could be considered as a potential anti-restenosis supplement.
Authors: F Cipollone; M Marini; M Fazia; B Pini; A Iezzi; M Reale; L Paloscia; G Materazzo; E D'Annunzio; P Conti; F Chiarelli; F Cuccurullo; A Mezzetti Journal: Arterioscler Thromb Vasc Biol Date: 2001-03 Impact factor: 8.311
Authors: A Buffon; G Liuzzo; L M Biasucci; P Pasqualetti; V Ramazzotti; A G Rebuzzi; F Crea; A Maseri Journal: J Am Coll Cardiol Date: 1999-11-01 Impact factor: 24.094