Ferulic acid induces mTor inactivation in cultured mammalian cells
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概要
- 論文の詳細を見る
Ferulic acid (FA), a naturally occurring polyphenol abundant in vegetables and rice bran, is known to possess a potent antioxidant activity, thereby protecting cells from oxidative stress. In the present study, we show that in addition to its known anti-oxidant activity, ferulic acid exerts substantial inhibitory activity on cellular mTor-signaling pathways. In HeLa cells and mouse primary hepatocytes cultured with conventional nutrient-rich media, ferulic acid (1 mM) elicited dephosphorylation of S6 kinase and its substrate ribosomal S6. The dephosphorylating activity of ferulic acid was almost comparable to that of rapamycin, an established mTor inhibitor (TORC1). We next investigated the effect of ferulic acid on autophagy, a major cellular degradative process, which significantly contributes to the maintenance of cell homeostasis. Using a conventional GFP-LC3 dot assay to evaluate autophagy flux, we showed that ferulic acid caused a significant increase in GFP-LC3 dots under serum-rich conditions in HeLa cells. The enhancement of autophagic flux by ferulic acid was almost equivalent to that of rapamycin. Furthermore, ferulic acid significantly enhanced autophagic degradation of 14C-leucine-labeled long-lived proteins of cultured mouse hepatocytes under nutrient-rich conditions, but not nutrient-deprived conditions. These results indicate that ferulic acid is almost the equivalent of rapamycin in the ability to inhibit mTor (TORC1), which makes it a potent activator of basal autophagy.
著者
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Furuya Norihiko
Department Of Applied Biological Chemistry Faculty Of Agriculture Niigata University
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Ezaki Junji
Department Of Biochemistry Juntendo University Faculty Of Medicine
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Ueno Takashi
Department Of Applied Chemistry Faculty Of Science And Engineering Ritsumeikan University
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UENO Takashi
Department of Biochemistry, Juntendo University School of Medicine
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Furuya Norihiko
Department of Biochemistry, Juntendo University School of Medicine
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Bian Zehua
Department of Biochemistry, Juntendo University School of Medicine
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Zheng Dong-Mei
Department of Biochemistry, Juntendo University School of Medicine
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Trejo Juan
Department of Biochemistry, Juntendo University School of Medicine
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Tada Norihiro
Division of Genome Research, Research Institute for Diseases of Old Ages, Juntendo University School of Medicine
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