Journal
JOURNAL OF ETHNOPHARMACOLOGY
Volume 150, Issue 3, Pages 875-885Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2013.09.039
Keywords
Ganoderma lucidum; Ganodermanontriol; Heme oxygenase-1; Hepatoprotective activity; Oxidative stress
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Funding
- NAFOSTED [106.99-2011.47]
- Basic Science Research Program through National Research Foundation of Korea (NRF)
- Priority Research Centers Program through the National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology of Korea [2011-0024389, 2009-0093815]
- Global R&D Center (GRDC) Program through the NRF
- MEST
- KRIBB Research Initiative Program
- National Research Foundation of Korea [2011-0024389] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Ethnopharmacological relevance: Ganoderma lucidum (Fr.) Karst. (Ganodermataceae) is a mushroom which is used as a traditional remedy in the treatment of human diseases such as hepatitis, liver disorders, hypercholesterolemia, arthritis, bronchitis and tumorigenic diseases. This study targets the evaluation of hepatoprotective activity of ganodermanontriol, a sterol isolated from Ganoderma lucidum, and the investigation of its mechanism of action in Hepa1c1c7 and murine liver cells upon tert-butyl hydroperoxide (t-BHP)-induced inflammation. t-BHP was utilized to stimulate an anti-inflammatory reaction in the hepatic cell lines and murine hepatic tissue examined. Western blot and reverse transcription-quantitative polymerase chain reaction (RT-PCR) were used to estimate the expression of ganodermanontriol (GDT)-induced proteins, including heme oxidase-1 (HO-1) and mitogen-activated protein kinases (MAPKs) as well as the corresponding mRNA. Luciferase assays were conducted to evaluate the interaction between NF-E2-related factor-2 (Nrf-2), the antioxidant response element (ARE), and the promoter region of the HO-1 gene and subsequent gene expression. Biochemical markers for hepatotoxicity were monitored to assess whether GDT protected the cells from the t-BHP-mediated oxidative stimuli. Results: GDT induced HO-1 expression via the activation of Nrf-2 nuclear translocation and the subsequent transcription of the HO-1 gene in vitro and in vivo, which seemed to be regulated by phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) and p38 signaling pathways. GDT exhibited in vitro and in vivo hepatoprotective activity as determined by the lowered levels of hepatic enzymes and malondialdehydes and the elevated glutathione levels. Conclusions: This study validates the ethnopharmacological application of Ganoderma lucidum as a treatment for hepatic disorders. GOT induced in vitro and in vivo anti-inflammatory activity in t-BHP-damaged hepatic cells through the expression of HO-1, and in which PI3K/Akt and p38 kinases are involved. Our study motivates further research in the exploration of potent hepatoprotective agents from Ganoderma lucidum. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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