ReferenceID 3875
Butein inhibits ethanol-induced activation of liver stellate cells through TGF-β, NFκB, p38, and JNK signaling pathways and inhibition of oxidative stress
J Gastroenterol
BACKGROUND: Butein has been reported to prevent and partly reverse liver fibrosis in vivo; however, the mechanisms of its action are poorly understood. We, therefore, aimed to determine the antifibrotic potential of bute
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Record Fields
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- Reference Id
- 3875
- Evidence Id
- 20465
- Core Evidence Id
- 20465
- Source Reference Id
- 1039
- Herb2 Reference Id
- HBREF001766
- Subject Paper Key
- HBIN019083_22722906
- Pubmed Id
- 22722906
- Doi
- 10.1007/s00535-012-0619-7
- Paper Title
- Butein inhibits ethanol-induced activation of liver stellate cells through TGF-β, NFκB, p38, and JNK signaling pathways and inhibition of oxidative stress
- Paper Abstract
- BACKGROUND: Butein has been reported to prevent and partly reverse liver fibrosis in vivo; however, the mechanisms of its action are poorly understood. We, therefore, aimed to determine the antifibrotic potential of butein. METHODS: We assessed the influence of the incubation of hepatic stellate cells (HSCs) and hepatoma cells (HepG2) with butein on sensitivity to ethanol- or acetaldehyde-induced toxicity; the production of reactive oxygen species (ROS); the expression of markers of HSC activation, including smooth muscle α-actin (α-SMA) and procollagen I; and the production of transforming growth factor-β1 (TGF-β1), metalloproteinases-2 and -13 (MMP-2and MMP-13), and tissue inhibitors of metalloproteinases (TIMPs). The influence of butein on intracellular signals in HSCs; i.e., nuclear factor-κB (NFκB), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) induced by ethanol was estimated. RESULTS: Butein protected HSCs and HepG2 cells against ethanol toxicity by the inhibition of ethanol- or acetaldehyde-induced production of ROS when cells were incubated separately or in co-cultures; butein also inhibited HSC activation measured as the production of α-SMA and procollagen I. As well, butein downregulated ethanol- or acetaldehyde-induced HSC migration and the production of TGF-β, TIMP-1, and TIMP-2; decreased the activity of MMP-2; and increased the activity of MMP-13. In ethanol-induced HSCs, butein inhibited the activation of the p38 MAPK and JNK transduction pathways as well as significantly inhibiting the phosphorylation of NF κB inhibitor (IκB) and Smad3. CONCLUSIONS: The results indicated that butein inhibited ethanol- and acetaldehyde-induced activation of HSCs at different levels, acting as an antioxidant and inhibitor of ethanol-induced MAPK, TGF-β, and NFκB/IκB transduction signaling; this result makes butein a promising agent for antifibrotic therapies.
- Journal
- J Gastroenterol
- Publish Year
- 2013
- Experiment Subject
- hepatic stellate cells (hscs) and hepatoma cells (hepg2)
- Experiment Type
- Cell Experiment
- Phenotype Related
- Liver Fibrosis
- Paper Title Cn
- Paper Title En
- Butein inhibits ethanol-induced activation of liver stellate cells through TGF-β, NFκB, p38, and JNK signaling pathways and inhibition of oxidative stress
- Bilingual Status
- semi_complete