Open AccessEffects of dabigatran regulates no‑reflow phenomenon in acute myocardial infarction mice through anti‑inflammatory and anti‑oxidative activities and connective tissue growth factor expression
Author(s) -
KyungSik Song,
Yanshan Wang,
Jizhang Sheng,
Chunmei Ma,
Hongmei Li
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.7861
Subject(s) - ctgf , medicine , oxidative stress , connective tissue , transforming growth factor , pharmacology , growth factor , pathology , receptor
Pradaxa is a novel oral anticoagulant, which was originally used to prevent thrombosis following joint replacement surgery. The aim of the current study was to investigate the effect dabigatran on acute myocardial infarction through regulating no‑reflow phenomenon and oxidative stress, neutrophil intraplaque infiltration and apoptosis. In the present study, dabigatran significantly inhibited the infarct size, increased arterial pressure and reduced no‑reflow phenomenon in acute myocardial infarction (AMI) vehicle rabbits. Treatment with dabigatran significantly inhibited the P65 of nuclear factor κB, tumor necrosis factor α, interleukin (IL)‑1β and IL‑6 activities and significantly enhanced the catalase and superoxide dismutase activities in the AMI rabbits. In addition, dabigatran significantly suppressed inducible nitric oxide synthase (iNOS), collagen I, transforming growth factor β1 (TGF‑β1), α‑smooth muscle actin (α‑SMA) and connective tissue growth factor (CTGF) protein expression in AMI rabbits. Taken together, these results suggest that the effects of dabigatran inhibit no‑reflow phenomenon, infarct size and enhance arterial pressure in AMI through anti‑inflammatory and anti‑oxidative activity, and regulating iNOS, collagen I, TGF‑β1, α‑SMA and CTGF protein expression in AMI rabbits.