Planta Med 1998; 64(7): 607-611
DOI: 10.1055/s-2006-957531
Paper
Pharmacology
© Georg Thieme Verlag Stuttgart · New York

Myocardial Protective Effect of an Anthraquinone-Containing Extract of Polygonum multiflorum Ex Vivo

T. K. Yim1 , W. K. Wu2 , D. H. F. Mak2 , K. M. Ko1 , 2
  • 1Department of Biochemistry, The Hong Kong University of Science & Technology, Clear Water Bay, Hong Kong, China
  • 2Hong Kong Traditional Chinese Medicine Research Center, The Hong Kong University of Science & Technology, Clear Water Bay, Hong Kong, China
Further Information

Publication History

1997

1998

Publication Date:
04 January 2007 (online)

Abstract

An ethyl acetate extract of Polygonum multiflorum Thunb. (PME) was fractionated into an anthraquinone-containing (PME-I) and a non-anthraquinone-containing (PME-II) fraction. The effects of PME and its related extracts pretreatment on myocardial ischemia-reperfusion (IR) injury in isolated perfused rat hearts were examined. Pretreatment with PME extract or its anthraquinone-containing fraction produced a dose-dependent protection against myocardial IR injury, as evidenced by a significant decrease in the extent of LDH leakage as well as an improvement in contractile force recovery. The myocardial protection was found to be associated with an enhancement in myocardial glutathione antioxidant status, as indicated by significant reductions in both the extent of IR-induced reduced glutathione (GSH) depletion and inhibition of Se-glutathione peroxidase (GPX) and glutathione reductase (GRD) activities. Both α-tocopherol acetate (VE) and emodin (EMD) pretreatments protected against IR-induced myocardial injury as assessed by the decrease in the extent of LDH leakage. But the contractile force recovery of the ischemic-reperfused hearts prepared from VE or EMD pretreated animals was not improved. The more complete myocardial protection afforded by the anthraquinone-containing fraction of PME extract may be related to its ability to sustain the glutathione antioxidant status under the condition of IR-induced oxidative stress.

    >