Effect of Ganoderma Lucidum Pharmacopuncture on Chronic Liver Injury in Rats

Objectives : Alcohol-related liver disease is a major cause of morbidity and mortality worldwide. The present study was undertaken to determine whether Ganoderma lucidum pharmaco- puncture(GLP) could protect against chronic liver injury induced by ethanol intoxication in rats. Methods : Sprague-Dawl...

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Bibliographic Details
Published inJournal of acupuncture research pp. 13 - 22
Main Authors 장선희, 윤현민, 김범회, 장경전, 김철홍
Format Journal Article
LanguageEnglish
Published 대한침구의학회 01.03.2015
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ISSN2586-288X
2586-2898

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Summary:Objectives : Alcohol-related liver disease is a major cause of morbidity and mortality worldwide. The present study was undertaken to determine whether Ganoderma lucidum pharmaco- puncture(GLP) could protect against chronic liver injury induced by ethanol intoxication in rats. Methods : Sprague-Dawley rats were divided into 4 groups: normal, control, normal saline pharmacopuncture(NP), and GLP, with 8 animals in each. Each group, except normal, received ethanol orally. The NP and GLP groups were treated daily with NP and GLP respectively. The control group was not treated. All rats except the normal group were intoxicated for 4 weeks by oral administration of EtOH(6 g/kg BW). Two acupuncture points were used: Qimen(LR14) and Taechung(LR3). Body weight, histopathological analysis, liver function, activities of antioxidant enzymes, and immunohistochemistry were assessed. Results : GLP reduced the histological changes due to chronic liver injury induced by EtOH and significantly reduced the increase in the alanine aminotransferase(ALT) and aspartate aminotransferase(AST) enzymes. It significantly reversed the superoxide dismutase(SOD) and the catalase activities(CAT). It also significantly decreased BAX and increased Bcl-2 immuno- reactivity expression. Conclusions : This study showed the protective efficacy of GLP against EtOH-induced chronic liver injury in SD rats by modulating ethanol metabolizing enzymes activity, attenuating oxidative stress, and inhibiting mitochondrial damage-mediated apoptosis. KCI Citation Count: 1
Bibliography:G704-000258.2015.32.1.006
ISSN:2586-288X
2586-2898