Study on the relationship of cPLA2, CK-MB, and membrane phospholipid content in acute myocardial infarction
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Li Wei-hua Han Jun-yu Sun Chang-qing Guo Yong-jun Xie Qiang Lin Kai-min Wu Rong Zhao Yan Lin Lin
- چاپ و سال / کشور: 2010
Description
Increased plasma creatine kinase-myoglobin (CK-MB) occurs in patients with acute myocardial infarction (AMI), but its underlying relationship with cytosolic phospholipase A2 (cPLA2) is poorly understood. In the present study we sought to determine cPLA2 activation and its relationship with plasma and myocardial CKMB level and membrane phospholipids (PLs) in an animal model of AMI. AMI was induced in 60 male Sprague- Dawley rats by ligating the left anterior descending of coronary artery. Rats were randomized into six groups at 0 (sham group), 1, 2, 4, 6, and 12 h after AMI onset (ten rats in each group). cPLA2 was detected by reverse transcription polymerase chain reaction and immunohistochemical staining for mRNA and protein expression, respectively. Plasma and myocardial CK-MB activity were measured by inhibition kinetics, and membrane PLs were determined by phosphorus quantitative method. Myocardial cPLA2 expression increased from 1 h and reached a peak at 2 h after AMI onset (p\0.01) followed by a decrease but still remained high, whereas plasma CK-MB significantly increased in rats from 4 h after the onset of AMI (p\0.05). During the first 6 h of AMI, a negative correlation existed between myocardial cPLA2 and membrane PLs (r = -0.504, p\0.01), whereas myocardial cPLA2 levels were positively associated with plasma CK-MB (r = 0.741, p\0.01) but negatively correlated with myocardial CK-MB in AMI groups (r = -0.785, p\0.01). Myocardial cPLA2 level increased and is positively correlated with plasma CK-MB activity and negatively correlated with membrane phospholipid content in AMI rats at early stage.
Heart Vessels (2011) 26:64–68 DOI 10.1007/s00380-010-0031-2 Received: 3 September 2009 / Accepted: 7 February 2010 / Published online: 27 October 2010
