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没食子丙醇对心肌缺血再灌注损伤的保护作用与抑制髓过氧化物酶活性和炎症细胞浸润有关。

Protective effect of phloroglucinol against myocardial ischaemia-reperfusion injury is related to inhibition of myeloperoxidase activity and inflammatory cell infiltration.

机构信息

Department of Pharmacology, Central South University, Changsha, China.

出版信息

Clin Exp Pharmacol Physiol. 2011 Jan;38(1):27-33. doi: 10.1111/j.1440-1681.2010.05457.x.

DOI:10.1111/j.1440-1681.2010.05457.x
PMID:21039756
Abstract
  1. It has been shown that phloroglucinol has anti-inflammatory and anti-oxidant properties. Both inflammatory cell infiltration and myeloperoxidase (MPO) activation play an important role in myocardial reperfusion injury. The aim of the present study was to explore the effect of phloroglucinol on myocardial reperfusion injury and the mechanisms involved. 2. Anaesthetized rats were pretreated with phloroglucinol (15 or 30 mg/kg, i.g.) or vehicle (5 mmol/L carboxymethyl cellulose sodium) 30 min prior to experimentation. The left main coronary artery was subjected to 1 h occlusion followed by 3 h reperfusion. Infarct size, the release of creatine kinase (CK), inflammatory cell infiltration, MPO activity and protein content, catalase in the blood and myocardium, and myocardial apoptosis were measured. 3. Following myocardial ischaemia and reperfusion in vehicle-treated rats, infarct size was 43.5 ± 3.7% (relative to the area at risk). Accompanying detrimental changes included elevated CK, enhanced inflammatory cell infiltration, high numbers of myocardial apoptotic cells, elevated caspase 3 activity, increased MPO activity and content in the plasma and myocardium and reduced catalase activity. These effects were attenuated by pretreatment with both doses of phloroglucinol (15 and 30 mg/kg, i.g.). 4. The results of the present study suggest that phloroglucinol protects the myocardium against ischaemia-reperfusion injury in rats and that its beneficial effects are related to inhibition of MPO activity and inflammatory cell infiltration.
摘要
  1. 已经表明,间苯三酚具有抗炎和抗氧化特性。炎症细胞浸润和髓过氧化物酶(MPO)激活在心肌再灌注损伤中起着重要作用。本研究旨在探讨间苯三酚对心肌再灌注损伤的影响及其机制。

  2. 麻醉大鼠在实验前 30 分钟用间苯三酚(15 或 30mg/kg,ig)或载体(5mmol/L 羧甲基纤维素钠)预处理。左冠状动脉主干闭塞 1 小时,再灌注 3 小时。测量梗死面积、肌酸激酶(CK)释放、炎症细胞浸润、MPO 活性和蛋白含量、血液和心肌中的过氧化氢酶以及心肌细胞凋亡。

  3. 在载体处理的大鼠心肌缺血再灌注后,梗死面积为 43.5±3.7%(相对于危险区域)。伴随的有害变化包括 CK 升高、炎症细胞浸润增强、心肌细胞凋亡增加、caspase 3 活性升高、血浆和心肌中 MPO 活性和含量增加以及过氧化氢酶活性降低。两种剂量的间苯三酚(15 和 30mg/kg,ig)预处理均可减轻这些影响。

  4. 本研究结果表明,间苯三酚对大鼠心肌缺血再灌注损伤具有保护作用,其有益作用与抑制 MPO 活性和炎症细胞浸润有关。

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