The fruits of Ligustrum lucidum Ait. (FLL) were fractionated into petroleum ether (FLL-Pe), chloroform (FLL-Ch), butanol (FLL-Bu) and aqueous (FLL-Aq) fractions, of which FLL-Ch and FLL-Bu were found to be enriched with oleanolic acid (OLA). The in vivo antioxidant activities of various FLL fractions and OLA were assessed by examining the effect on carbon tetrachloride (CCl(4))-induced hepatotoxicity in mice. Pretreatment of animals with various FLL fractions could protect against CCl(4)-induced hepatotoxicity to a varying degree, with OLA-enriched FLL-Bu and FLL-Ch being more potent. However, a mortality rate of 60% was observed in the FLL-Ch pretreated and CCl(4)-intoxicated mice. OLA pretreatment also produced a dose-dependent protection against CCl(4) hepatotoxicity. The hepatoprotection afforded by FLL-Bu or OLA pretreatment was associated with an enhancement of hepatic-glutathione regeneration capacity (GRC). In contrast, the inability of FLL-Aq pretreatment to enhance hepatic GRC resulted in a failure to prevent CCl(4)-induced hepatic injury. The results suggest that the hepatoprotective action afforded by OLA-enriched FLL-Bu or OLA pretreatment may be mainly mediated by the enhancement of hepatic GRC, particularly under conditions of CCl(4)-induced oxidative stress.
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 alpha-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.
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