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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2016.1
- 수록면
- 59 - 69 (11page)
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이 논문의 연구 히스토리 (2)
2016
Cytoprotective effect of ganoderma lucidum ethanol extract against oxidative stress in C2C12 myoblasts through upregulation of Nrf2/HO-1 pathway
이유환
한의학과
2016.01
학위논문
Ethanol Extract of Ganoderma lucidum Augments Cellular Anti-oxidant Defense through Activation of Nrf2/HO-1
이유환
,
김정희
,
송춘호
외 5명
Journal of Pharmacopuncture
2016.01
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Objectives: The mushroom Ganoderma lucidum has been widely used as a traditional herbal medicine for many years. Although several studies have focused on the anti-oxidative activity of this mushroom, the molecular mechanisms underlying its activity have not yet been clearly established. The present study investigated the cytoprotective effect of ethanol extract of Ganoderma lucidum (EGL) against oxidative stress (hydrogen peroxide, H2O2) and elucidated the underlying mechanisms in a C2C12 myoblast cell line.
Methods: Oxidative stress markers were determined by using the comet assay to measure reactive oxygen species (ROS) generation and deoxyribonucleic acid (DNA) damage. Cell viability and Western blotting analyses were employed to evaluate the cellular response to EGL and H2O2 in C2C12 cells. Transfection with nuclear factor erythroid 2-related factor 2 (Nrf2)-specific small interfering ribonucleic acid (siRNA) was conducted to understand the relationship between Nrf2 expression and H2O2-induced growth inhibition.
Results: The results showed that EGL effectively inhibited H2O2-induced growth and the generation of ROS.
EGL markedly suppressed H2O2-induced comet-like DNA formation and phosphorylation of histone H2AX at serine 139 (p-γH2AX), a widely used marker of DNA damage, suggesting that EGL prevented H2O2-induced DNA damage. Furthermore, the EGL treatment effectively induced the expression of Nrf2, as well as heme oxygenase-1 (HO-1), with parallel phosphorylation and nuclear translocation of Nrf2 in the C2C12 myoblasts.
However, zinc protoporphyrin IX, a HO-1 inhibitor, significantly abolished the protective effects of EGL against H2O2-induced accumulation of ROS and reduced cell growth. Notably, transient transfection with Nrf2-specific siRNA attenuated the cytoprotective effects and HO-1 induction by EGL, indicating that EGL induced the expression of HO-1 in an Nrf2-dependent manner.
Conclusion: Collectively, these results demonstrate that EGL augments the cellular anti-oxidant defense capacity through activation of Nrf2/HO-1, thereby protecting C2C12 myoblasts from H2O2-induced oxidative cytotoxicity.
목차
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참고문헌 (40)
참고문헌 신청
Szczesny B / 2013 / Deficiency in repair of the mitochondrial genome sensitizes proliferating myoblasts to oxidative damage / PLoS One 8(9):e75201
Miller CJ / 2012 / Disruption of Nrf2/ARE signaling impairs antioxidant mechanisms and promotes cell degradation pathways in aged skeletal muscle / Biochim Biophys Acta 1822(6):1038~1050
Ji LL / 2006 / Exercise and hormesis : activation of cellular antioxidant signaling pathway / Ann N Y Acad Sci 1067:425~435
Forman HJ / 2007 / Use and abuse of exogenous H2O2 in studies of signal transduction / Free Radic Biol Med 42(7):926~932
Halliwell B / 2006 / Oxidative stress and neurodegeneration : where are we now? / J Neurochem 97(6):1634~1658
Miller CJ / 2012 / Disruption of Nrf2/ARE signaling impairs antioxidant mechanisms and promotes cell degradation pathways in aged skeletal muscle / Biochim Biophys Acta 1822(6):1038~1050
Ji LL / 2006 / Exercise and hormesis : activation of cellular antioxidant signaling pathway / Ann N Y Acad Sci 1067:425~435
Forman HJ / 2007 / Use and abuse of exogenous H2O2 in studies of signal transduction / Free Radic Biol Med 42(7):926~932
Halliwell B / 2006 / Oxidative stress and neurodegeneration : where are we now? / J Neurochem 97(6):1634~1658
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