作者
Carlo Marchetti, Stefano Toldo, Jeremy Chojnacki, Eleonora Mezzaroma, Kai Liu, Fadi N Salloum, Andrea Nordio, Salvatore Carbone, Adolfo Gabriele Mauro, Anindita Das, Ankit A Zalavadia, Matthew S Halquist, Massimo Federici, Benjamin W Van Tassell, Shijun Zhang, Antonio Abbate
发表日期
2015/7/1
期刊
Journal of cardiovascular pharmacology
卷号
66
期号
1
页码范围
1-8
出版商
LWW
简介
Background:
Sterile inflammation resulting from myocardial injury activates the NLRP3 inflammasome and amplifies the inflammatory response mediating further damage.
Methods:
We used 2 experimental models of ischemic injury (acute myocardial infarction [AMI] with and without reperfusion) and a model of nonischemic injury due to doxorubicin 10 mg/kg to determine whether the NLRP3 inflammasome preserved cardiac function after injury.
Results:
Treatment with the NLRP3 inflammasome inhibitor in the reperfused AMI model caused a significant reduction in infarct size measured at pathology or as serum cardiac troponin I level (− 56% and− 82%, respectively, both P< 0.001) and preserved left ventricular fractional shortening (LVFS, 31±2 vs. vehicle 26%±1%, P= 0.003). In the non-reperfused AMI model, treatment with the NLRP3 inhibitor significantly limited LV systolic dysfunction at 7 days (LVFS of 20±2 vs …
学术搜索中的文章
C Marchetti, S Toldo, J Chojnacki, E Mezzaroma, K Liu… - Journal of cardiovascular pharmacology, 2015