Abstract：
:Acute myocardial infarction (AMI) is associated with inflammation and apoptosis. Emodin plays an anti-inflammatory role in several inflammatory diseases. Recent studies have demonstrated that emodin protects against myocardial ischemia/reperfusion injury. However, its mechanism underlying its effects remains unknown. In a murine model of AMI, based on ligation of the left coronary artery, administration of emodin reduced myocardial infarct size (MIS) in a dose-dependent manner. Emodin significantly suppressed TNF-alpha expression and NF-kappaB activation in the local myocardial infarction area. Treatment with emodin inhibited myocardial cell apoptosis by inhibiting caspase-3 activation. Therefore, these studies demonstrate that emodin protects against myocardial cell injury via suppression of local inflammation and apoptosis.
journal_name
Life Scijournal_title
Life sciencesauthors
Wu Y,Tu X,Lin G,Xia H,Huang H,Wan J,Cheng Z,Liu M,Chen G,Zhang H,Fu J,Liu Q,Liu DXdoi
10.1016/j.lfs.2007.08.040subject
Has Abstractpub_date
2007-10-13 00:00:00pages
1332-8issue
17-18eissn
0024-3205issn
1879-0631pii
S0024-3205(07)00641-8journal_volume
81pub_type
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