| Title |
Genistein suppresses tumor necrosis factor α-induced inflammation via modulating reactive oxygen species/Akt/nuclear factor ΚB and adenosine monophosphate-activated protein kinase signal pathways in human synoviocyte MH7A cells
|
|---|---|
| Published in |
Drug Design, Development and Therapy, March 2014
|
| DOI | 10.2147/dddt.s52354 |
| Pubmed ID | |
| Authors |
Jinchao Li, Jun Li, Ye Yue, Yiping Hu, Wenxiang Cheng, Ruoxi Liu, Xiaohua Pan, Peng Zhang |
| Abstract |
Genistein, an isoflavone derivative found in soy, is known as a promising treatment for rheumatoid arthritis (RA). However, the detailed molecular mechanism of genistein in suppression of proinflammatory cytokine production remains ambiguous. The aim of this work was to evaluate the signal pathway by which genistein modulates inflammatory cytokine expression. MH7A cells were stimulated with tumor necrosis factor (TNF)-α and incubated with genistein, and interleukin (IL)-1β, IL-6, and IL-8 production was measured by enzyme-linked immunosorbent assay. Nuclear translocation of nuclear factor (NF)-κB was measured by a confocal fluorescence microscopy. The intracellular accumulation of reactive oxygen species (ROS) was monitored using the fluorescent probe 5-6-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate. Signal-transduction protein expression was measured by Western blot. Genistein decreased the secretion of IL-1β, IL-6, and IL-8 from TNF-α-stimulated MH7A cells in a dose-dependent manner. Genistein prevented TNF-α-induced NF-κB translocation as well as phosphorylation of IκB kinase-α/β and IκBα, and also suppressed TNF-α-induced AMPK inhibition. The production of IL-1β, IL-6, and IL-8 induced by TNF-α was decreased by the phosphatidylinositol-3 kinase inhibitor LY294002, suggesting that inhibition of Akt activation might inhibit IL-1β, IL-6, and IL-8 production induced by TNF-α. In addition, we also found that pretreatment with the adenosine monophosphate-activated protein kinase (AMPK) agonist 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside obviously inhibited TNF-α-induced proinflammatory cytokine production. These observations suggest that the inhibitory effect of genistein on TNF-α-induced proinflammatory cytokine production is dependent on AMPK activation. These findings indicate that genistein suppressed TNF-α-induced inflammation by inhibiting the ROS/Akt/NF-κB pathway and promoting AMPK activation in MH7A cells. |
X Demographics
The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Practitioners (doctors, other healthcare professionals) | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 59 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| France | 1 | 2% |
| Unknown | 58 | 98% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 8 | 14% |
| Student > Bachelor | 7 | 12% |
| Student > Doctoral Student | 6 | 10% |
| Student > Master | 6 | 10% |
| Researcher | 4 | 7% |
| Other | 10 | 17% |
| Unknown | 18 | 31% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 13 | 22% |
| Biochemistry, Genetics and Molecular Biology | 7 | 12% |
| Pharmacology, Toxicology and Pharmaceutical Science | 5 | 8% |
| Neuroscience | 3 | 5% |
| Agricultural and Biological Sciences | 3 | 5% |
| Other | 9 | 15% |
| Unknown | 19 | 32% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 18 March 2014.
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#22,756,649
of 25,371,288 outputs
Outputs from Drug Design, Development and Therapy
#1,754
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Outputs of similar age
#206,406
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Outputs of similar age from Drug Design, Development and Therapy
#14
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