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Aim:To observe neuroprotective effects of raw and roasted licorice against hy-poxia and ischemic damage.Methods:When elucidating the protective effects ofraw and roasted licorice,we analyzed the lactate dehydrogenase (LDH) releaseusing PC12 cells after hypoxia in an in vitro study and after transient forebrainischemia in an in vivo study on Mongolian gerbils.Results:Raw and roastedlicorice significantly reduced LDH release from PC12 cells exposed to an hypoxicchamber for 1h.In the roasted licorice-treated group,the decrease of LDH releasewas more pronounced compared to that of the raw licorice-treated group.Inroasted licorice-treated animals,approximately 66%-71% of CA1 pyramidal cellsin the ischemic hippocampus were stained with cresyl violet compared to thecontrol group.However,in the raw licorice-treated animals,no significantneuroprotection against ischemic damage was shown.In addition,ischemic ani-mals in roasted licorice-treated group maintained the Cu,Zn-superoxide dismutase(SOD1) activity and protein levels compared to the control group,while in rawlicorice-treated group SOD1 activity and protein levels were reduced significantly.High pressure liquid chromatography analysis showed that non-polar compoundscontaining glycyrrhizin-degraded products,such as glycyrrhetinic acid (GA) andglycyrrhetinic acid monoglucuronide (GM),were increased in roasted licorice.Conclusion:Roasted licorice had neuroprotective effects against ischemic dam-age by maintaining the SOD1 levels.In addition,the difference in protectiveability between raw and roasted licorice may be associated with non-polarcompounds,such as GA and GM.
Aim: To observe neuroprotective effects of raw and roasted licorice against hy-poxia and ischemic damage. Methods: When elucidating the protective effects ofraw and roasted licorice, we analyzed the lactate dehydrogenase (LDH) release using PC12 cells after hypoxia in an in vitro study and after transient forebrain ischemia in an in vivo study on Mongolian gerbils. Results: Raw and roasted licorice significantly reduced LDH release from PC12 cells exposed to an hypoxic chamber for 1 h. In the roasted licorice-treated group, the decrease of LDH release was more pronounced to that of the raw licorice-treated group.In broasted licorice-treated animals, approximately 66% -71% of CA1 pyramidal cells in the ischemic hippocampus were stained with cresyl violet compared to the control group. Despite, in the raw licorice-treated animals, no significantneuroprotection against ischemic damage was shown.In addition, ischemic ani-mals in roasted licorice-treated group maintained the Cu, Zn-superoxide dismutase (SOD 1) activity and protein levels compared to the control group, while in rawlicorice-treated group SOD1 activity and protein levels were reduced significantly. High pressure liquid chromatography analysis showed that non-polar compoundscontaining glycyrrhizin-degraded products, such as glycyrrhetinic acid (GA) andglycyrrhetinic acid monoglucuronide (GM), were increased in roasted licorice. Conlusion: Roasted licorice had neuroprotective effects against ischemic dam-age by maintaining the level of protective activity between raw and roasted licorice may be associated with non-polar compounds , such as GA and GM.