Urinary trypsin inhibitor reduced inflammatory response after stent injury in minipig.

This study investigated whether urinary trypsin inhibitor (UTI) inhibits neointimal formation by reducing inflammatory response after stent injury. Twenty minipigs having undergone oversized bare material stent implantation in the left anterior descending artery were randomly subdivided into two groups: a UTI group (n=10) and a control group (n=10). Two systemic markers of inflammation (serum macrophage chemoattractant protein-1 and interleukin-6 levels measured by ELISA) were increased after stent implantation, and two days after stem implantation, their levels were positively correlated with the maximal percentage of area stenosis on day 28 (r(2)=0.889 and 0.743, respectively). This effect was abolished by UTI administration. Twenty-eight days after implantation, morphometric analysis of the stented arteries revealed significantly reduced luminal stenosis (38±6% vs. 64±12%, P<0.05), a neointimal area (3.22±0.57 mm(2) vs. 5.21±1.04 mm(2), P<0.05), neointimal thickness (0.31±0.13 mm vs. 0.46±0.16 mm, P<0.05), and an inflammatory score of 1.02±0.05 vs. 1.30±0.08 in UTI-treated animals as compared with controls. Twenty-eight days after stenting, arterial nuclear factor-κB expression was 36.93±7.16% in all of the cells in controls and 23.32±4.54% in UTI-treated minipigs. UTI could reduce neointimal formation after stenting by inhibiting the local and the systemic inflammatory response. Percutaneous coronary intervention could benefit from precocious anti-inflammatory treatment.