A rat model of myocardial ischemia-reperfusion (IR) injury was used for assessing the antioxidant activity of an ethylacetate extract of Polvgonum multiflorum (PME) and Schisandrin B (Sch B), a dibenzocyclooctadiene derivative isolated from Fructus Schisandrae, in the myocardium. The results have demonstrated the protective effect of PME and Sch B on the myocardium against IR injury, as evidenced by a significant decrease in the extent of lactate dehydrogenase leakage as well as an improvement in contractile force recovery....[ Read more ]

A rat model of myocardial ischemia-reperfusion (IR) injury was used for assessing the antioxidant activity of an ethylacetate extract of Polvgonum multiflorum (PME) and Schisandrin B (Sch B), a dibenzocyclooctadiene derivative isolated from Fructus Schisandrae, in the myocardium. The results have demonstrated the protective effect of PME and Sch B on the myocardium against IR injury, as evidenced by a significant decrease in the extent of lactate dehydrogenase leakage as well as an improvement in contractile force recovery.

Pretreatment with PME extract or its anthraquinone (e.g. emodin)-containing fraction (PME-I) produced a dose-dependent protection against myocardial IR injury. However, the contractile force recovery of the ischemic-reperfused hearts prepared from emodin (EMD) pretreated animals was not improved. It is possible that anthraquinone compounds other than EMD present in PME and PME-I produced the inotropic effect and/or EMD and other anthraquinones present in PME and PME-I extracts act synergistically in producing myocardial protection against IR-induced oxidative stress.

While perfusing the previously ischemic myocardium with free radcial scavenging antioxidants such as Trolox and ascorbic acid protected against IR injury, perfusion with liposome-entrapped Sch B during reperfusion did not show any protection. In contrast, pretreatment with Sch B protected against IR-induced myocardial damage in a dose-dependent manner. The myocardial protection was associated with an enhancement in myocardial glutathione antioxidant status, as indicated by significant reductions in both the extent of IR-induced reduced glutathione depletion and inhibition of Se-glutathione peroxidase and glutathione reducatse activities. In contrast, the inability of Dimethyl-4,-4'-dimethoxy-5,6,5',6'-dimethylene-dioxy- biphenyl-2,2'-bicarboxylate pretreatment to enhance myocardial glutathione antioxidant status resulted in a failure in preventing IR injury. The ensemble of results suggests that the myocardial protection afforded by Sch B pretreatment, which was unlikely due to free radical scavenging action, may be mainly mediated by the enhancement of myocardial glutathione antioxidant status. Preliminary structure-activity relationship studies indicated that both the methylenedioxy group and the cyclooctadiene ring are important structural determinants of the schisandrin molecule in enhancing myocardial glutathione status in ischemic-reperfused hearts.