Abstract
Previous investigations have suggested that tumor necrosis factor-alpha (INF-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/dtmax, 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 1 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.
Original language | English |
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Pages (from-to) | 818-822 |
Number of pages | 5 |
Journal | Planta Medica |
Volume | 70 |
Issue number | 9 |
DOIs | |
State | Published - Sep 2004 |
Keywords
- 1,1-diphenyl-2-picrylhydrazyl
- Apiaceae
- Ligusticum wallichii
- Ligustrazine
- Myocardial ischemia-reperfusion injury
- Rat isolated heart
- Tumor necrosis factor-alpha