Rotundarpene inhibits TNF-alpha-induced activation of the Akt, mTOR, and NF-kappa B pathways, and the JNK and p38 associated with production of reactive oxygen species
- Authors
- Kim, Arum; Nam, Yoon Jeong; Shin, Yong Kyoo; Lee, Min Sung; Sohn, Dong Suep; Lee, Chung Soo
- Issue Date
- Oct-2017
- Publisher
- SPRINGER
- Keywords
- Keratinocytes; Tumor necrosis factor-alpha; Rotundarpene; Inflammatory mediator production; Akt, mTOR and NF-kappa B pathways; JNK and p38-MAPK
- Citation
- MOLECULAR AND CELLULAR BIOCHEMISTRY, v.434, no.1-2, pp 113 - 125
- Pages
- 13
- Journal Title
- MOLECULAR AND CELLULAR BIOCHEMISTRY
- Volume
- 434
- Number
- 1-2
- Start Page
- 113
- End Page
- 125
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/3811
- DOI
- 10.1007/s11010-017-3041-x
- ISSN
- 0300-8177
1573-4919
- Abstract
- Ilex Rotunda Thunb has been shown to have anti-inflammatory and antioxidant effects. In human keratinocytes, we investigated the effect of rotundarpene (4-caffeoyl-3-methyl-but-2-ene-1,4-diol) on the TNF-alpha-stimulated production of inflammatory mediators in relation to the Akt, mTOR, and NF-kappa B pathways, and the JNK and p38-MAPK. Rotundarpene, Akt inhibitor, Bay 11-7085, rapamycin, and N-acetylcysteine inhibited the TNF-alpha-stimulated production of cytokines and chemokines, increase in the levels of p-Akt and mTOR, activation of NF-kappa B, and production of reactive oxygen species in keratinocytes. TNF-alpha treatment induced phosphorylation of the JNK and p38-MAPK. Inhibitors of the c-JNK (SP600125) and p38-MAPK (SB203580) reduced the TNF-alpha-induced production of inflammatory mediators, binding of NF-kappa B to DNA, and activation of the JNK and p38-MAPK in keratinocytes. The results show that rotundarpene may reduce the TNF-alpha-stimulated inflammatory mediator production by suppressing the reactive oxygen species-dependent activation of the Akt, mTOR, and NF-kappa B pathways, and activation of the JNK and p38-MAPK in human keratinocytes. Additionally, rotundarpene appears to attenuate the Akt, mTOR, and NF-kappa B pathways and the JNK and p38-MAPK-mediated inflammatory skin diseases.
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