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Tussilagonone-induced Nrf2 pathway activation protects HepG2 cells from oxidative injury

Title
Tussilagonone-induced Nrf2 pathway activation protects HepG2 cells from oxidative injury
Authors
Lee K.-M.Kwon T.Y.Kang U.Seo E.K.Yun J.H.Nho C.W.Kim Y.S.
Ewha Authors
서은경
SCOPUS Author ID
서은경scopus
Issue Date
2017
Journal Title
Food and Chemical Toxicology
ISSN
0278-6915JCR Link
Citation
vol. 108, pp. 120 - 127
Keywords
ERK1/2Hepatoprotective effectNrf2Oxidative injuryTussilagonone
Publisher
Elsevier Ltd
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Tussilagonone is a compound derived from the medicinal plant Tussilago farfara L., which is used as a traditional medicine for respiratory diseases, including asthma and pneumonia. Recent reports suggest that tussilagonone exhibits anti-inflammatory effects; however, the scope of protective functions has not been elucidated yet. In this study, we demonstrate that tussilagonone enhances cellular detoxification by increasing quinone reductase activity in Hepa1c1c7 cells. In addition, tussilagonone decreased tert-butyl hydroperoxide(t-BHP)-induced ROS production and cell death, suggesting that it also acts as a potent antioxidant. To verify the molecular mechanism underlying tussilagonone activity, we examined the expression of nuclear factor erythroid 2-related factor 2(Nrf2)—a transcription factor that regulates antioxidant protein expression—in HepG2 cells. Significantly, these results showed that tussilagonone induces Nrf2 activation and nuclear accumulation, resulting in the upregulation of the detoxifying enzymes NAD(P)H quinone dehydrogenase 1(NQO1) and heme oxygenase-1(HO-1) that protect cells from oxidative stress. Further molecular analyses revealed that tussilagonone-induced Nrf2 activation was mediated by ERK1/2 in HepG2 cells. Collectively, these data indicate that tussilagonone attenuates t-BHP-induced ROS and activates quinone reductase activity via Nrf2 pathway activation and target gene expression, and thereby acts as an antioxidant that protects HepG2 cells from oxidative stress and associated damage. © 2017 Elsevier Ltd
DOI
10.1016/j.fct.2017.07.035
Appears in Collections:
약학대학 > 약학과 > Journal papers
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