Effect of total peony glucoside pretreatment on NF-κB and ICAM-1 expression in myocardial tissue of rat with myocardial ischemia-reperfusion injury.
Early recovery of myocardial perfusion is beneficial for myocardial ischemia. However, ischemia-reperfusion (I/R) may exacerbate myocardial injury. Research shows that total peony glucoside (TPG) can inhibit ischemic myocardial cell apoptosis. However, whether it can ameliorate I/R injury remains poorly understood. This study explored the effect of TPG pretreatment on I/R, through nuclear factor-kappa B (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) expressions in I/R-affected myocardium. Healthy 7-week-old male Sprague Dawley rats were randomly categorized into sham operation (A), modeling (B), and 100, 200, and 400 mg/kg TPG pretreatment groups (C, D, and E, respectively), with 20 rats in each group. I/R rat models were designed by ligating left anterior descending coronary artery for 30 min to induce ischemia and for 120 min to induce reperfusion. Serum interleukin 6 (IL-6) and interleukin 8 (IL-8) levels were measured using enzyme linked immunosorbent assay. NF-κB and ICAM-1 mRNA and protein expressions were detected through RT-PCR and western blot analysis, respectively. Compared to group A, serum IL-6 and IL-8 levels of group B elevated significantly (P < 0.05), whereas NF-κB and ICAM-1 mRNA and protein expressions increased in the myocardium (P < 0.05). Serum IL-6 and IL-8 levels, and NF-κB and ICAM-1 mRNA and protein expressions, in myocardium of TPG groups reduced in a dose-dependent manner. Therefore, TPG pretreatment could alleviate myocardium reperfusion injury in I/R rat models by reducing NF-κB and ICAM-1 mRNA and protein expressions and cytokine secretions. This mechanism could be associated with the inhibition of NF-κB activation and downregulation of ICAM-1 expression.
The First College of Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.|Department of Cardiology, Xuzhou City TCM Hospital, Xuzhou, Jiangsu, China.
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Lu
Department of Cardiology, Xuzhou Central Hospital, Xuzhou, Jiangsu, China.
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Wei
Department of Cardiology, Xuzhou City TCM Hospital, Xuzhou, Jiangsu, China.
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Cao
Department of Cardiology, Xuzhou City TCM Hospital, Xuzhou, Jiangsu, China.
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Zhang
Department of Cardiology, Xuzhou City TCM Hospital, Xuzhou, Jiangsu, China.
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Liu
Department of Cardiology, Xuzhou City TCM Hospital, Xuzhou, Jiangsu, China.
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Liu
Department of Cardiology, Xuzhou City TCM Hospital, Xuzhou, Jiangsu, China.
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Wang
The First College of Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China xiangsingcheng@sina.com.|Department of Cardiology, Xuzhou Central Hospital, Xuzhou, Jiangsu, China xiangsingcheng@sina.com.
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Zhang
D000818:Animals; D004195:Disease Models, Animal; D005960:Glucosides / Q000494:pharmacology / Q000627:therapeutic use*; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics* / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000188:drug therapy* / Q000235:genetics* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D016328:NF-kappa B / Q000235:genetics* / Q000378:metabolism; D029596:Paeonia / Q000737:chemistry*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D017207:Rats, Sprague-Dawley
D005960:Glucosides; D015850:Interleukin-6; D016209:Interleukin-8; D016328:NF-kappa B; D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1