Possible Mechanism of Rottlerin Induced Modulation of Ischemia Reperfusion Injury in Isolated Rat Hearts

DOI Web Site Web Site 参考文献52件
  • Kaur Kamalpreet
    Department of Pharmaceutical Sciences and Drug Research, Punjabi University
  • Singh Manjeet
    Department of Pharmaceutical Sciences and Drug Research, Punjabi University
  • Singh Nirmal
    Department of Pharmaceutical Sciences and Drug Research, Punjabi University
  • Jaggi Amteshwar Singh
    Department of Pharmaceutical Sciences and Drug Research, Punjabi University

この論文をさがす

抄録

The present study was designed to investigate the modulatory effects of rottlerin on ischemia reperfusion induced myocardial injury. Isolated rat hearts were exposed to 30 min of global ischemia followed by 120 min of reperfusion using Langendorff apparatus. Myocardial injury was assessed in the terms of infarct size, release of lactate dehydrogenase (LDH), creatine kinase (CK) enzymes. Rottlerin, a selective PKCδ inhibitor, did not modulate ischemia-reperfusion (I/R) induced myocardial injury at low dose (3 μM). However, at moderate dose (6 μM) it significantly produced cardioprotective effects. On the contrary, rottlerin at high dose (12 μM) significantly enhanced I/R induced myocardial injury. However, administration of FR-167653 (1.1 μM, 2.2 μM), a selective p-38 mitogen activated protein kinase (p-38 MAPK) inhibitor, attenuated rottlerin (12 μM) mediated enhancement in I/R induced myocardial injury in a dose dependent manner. Per se administration of FR-167653 (1.1 μM, 2.2 μM) also attenuated I/R induced myocardial injury in a dose dependent manner. Pretreatment with rottlerin (6 μM) did not enhance the cardioprotective effects of FR-167653 (2.2 μM). It may be concluded that rottlerin mediated cardioprotective effects at moderate dose, possible due to inhibition of PKCδ; while at high dose it enhanced I/R induced myocardial injury which may be attributed to activation of p-38 MAPK.

収録刊行物

参考文献 (52)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ