Planta Med 2004; 70(9): 818-822
DOI: 10.1055/s-2004-827229
Original Paper
Pharmacology
© Georg Thieme Verlag KG Stuttgart · New York

The Protective Effects of Ligustrazine on Ischemia-Reperfusion and DPPH Free Radical-Induced Myocardial Injury in Isolated Rat Hearts

Yuan Zhou1 , Chang-Ping Hu2 , Pan-Yue Deng2 , Han-Wu Deng2 , Yuan-Jian Li2
  • 1Department of Pharmacology, Medical College, Hunan Normal University, Changsha, Hunan, P. R. China
  • 2Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, Hunan, P. R. China
Further Information

Publication History

Received: February 6, 2004

Accepted: May 15, 2004

Publication Date:
23 September 2004 (online)

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Abstract

Previous investigations have suggested that tumor necrosis factor-alpha (TNF-α) can contribute to myocardial damage during ischemia-reperfusion. In the present study, we examined whether the cardioprotective effects of ligustrazine are related to inhibition of TNF-α production in the rat models of ischemia-reperfusion and 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical-induced myocardial injury. Ischemia for 20 min and reperfusion for 40 min caused a decline in cardiac function (left ventricular pressure, ± dp/dt max, heart rate and coronary flow) and an increase in the release of creatine kinase in coronary effluent and the content of TNF-α in myocardial tissues. Similarly, perfusion with DPPH (100 nM) for 30 min significantly decreased cardiac function, and increased the release of creatine kinase and the content of TNF-α. Ligustrazine at the concentration of 40 or 80 mg/L markedly improved cardiac function and reduced the release of creatine kinase and the content of TNF-α in myocardial tissues in hearts subjected to ischemia-reperfusion or DPPH perfusion. These results suggest that the cardioprotection afforded by ligustrazine is related to a reduction of TNF-α content by inhibition of free radical production in isolated rat hearts.