Protective effects of ginsenosides on anoxia/reoxygenation of cultured rat myocytes and on reperfusion injuries against lipid peroxidation.

Abstract

Lactic acid dehydrogenases (LDH) release from cultured rat myocytes during anoxia and reoxygenation were significantly reduced by ginsenosides (G) and its components Rb+Ro, both in 83 micrograms/ml, but not by Rg. G in higher concentration (250 micrograms/ml) enhanced the LDH release. G and Rb+Ro both 8.3 micrograms/ml in the perfusate, also significantly reduced CPK release from isolated rat heart. Rb component 50 mg/kg protected rat myocardial infarct in vivo against lipid peroxidation signified by significant reduction of malondialdehyde (MDA) and increase of superoxide dismutase (SOD) in rat myocardium. It was concluded that G in adequate dose can protect myocyte anoxia and reoxygenation as well as reperfusion damage in isolated rat heart, and the mechanism of protection may partly attribute to its action on oxygen free radical formation and lipid peroxidation. The active components of myocardial protection are Rb+Ro, and not Rg.

• Authors: X Chen, Y J Li, H W Deng, B C Yang, D Y Li, N Shen
• Journal: Biomedica biochimica acta (Biomed Biochim Acta) Vol. 46 Issue 8-9 Pg. S646-9 ( 1987) ISSN: 0232-766X [Print] Germany
• PMID: 3435520 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Ginsenosides
• Lipid Peroxides
• Saponins
• Malondialdehyde
• L-Lactate Dehydrogenase
• Superoxide Dismutase

Topics

• Animals
• Cells, Cultured
• Coronary Disease (drug therapy, metabolism)
• Ginsenosides
• Hypoxia (metabolism)
• L-Lactate Dehydrogenase (metabolism)
• Lipid Peroxides (metabolism)
• Malondialdehyde (metabolism)
• Myocardium (metabolism)
• Rats
• Saponins (pharmacology)
• Superoxide Dismutase (metabolism)