| Title |
Protective effect of hydrogen sulfide on TNF-α and IFN-γ-induced injury of intestinal epithelial barrier function in Caco-2 monolayers
|
|---|---|
| Published in |
Inflammation Research, August 2015
|
| DOI | 10.1007/s00011-015-0862-5 |
| Pubmed ID | |
| Authors |
Shan-wen Chen, Jing Zhu, Shuai Zuo, Jun-ling Zhang, Zi-yi Chen, Guo-wei Chen, Xin Wang, Yi-sheng Pan, Yu-cun Liu, Peng-yuan Wang |
| Abstract |
Studies have verified the protective effect of Hydrogen Sulfide (H2S) on gastric ulcer and ulcerative colitis, but the mechanisms are not fully illustrated. In this study, the possible protective effect of H2S on TNF-α/IFN-γ induced barrier dysfunction was investigated in Caco-2 cell monolayers. The barrier function of Caco-2 monolayers was evaluated by measuring trans-epithelial electrical resistance (TEER) and FITC-Dextran 4 kDa (FD-4) trans-membrane flux. ZO-1 and Occludin were chosen as markers of the localization of tight junction (TJ) proteins for immunofluorescence. The expression of MLCK and phosphorylation level of myosin light chain (MLC) were measured by immunoblotting. The activation of NF-kB p65 was analyzed by EMSA and immunofluorescence. NaHS at 500uM significantly attenuated TNF-α/IFN-γ-indueced Caco-2 monolayer barrier injury. The increased expression of MLCK and increased phosphorylation level of MLC induced by TNF-α/IFN-γ was also inhibited significantly by NaHS. Additionally, NaHS inhibited TNF-α/IFN-γ induced activation and nuclear translocation of NF-kB p65. The present study reveals the protective effect of H2S on TNF-α and IFN-γ-induced injury of intestinal epithelial barrier function in Caco-2 monolayers and suggests that the suppression of MLCK-P-MLC signaling mediated by NF-kB P65 might be one of the mechanisms underlying the protective effect of H2S. |
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 % |
|---|---|---|
| Science communicators (journalists, bloggers, editors) | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 54 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 54 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 9 | 17% |
| Student > Postgraduate | 7 | 13% |
| Student > Bachelor | 6 | 11% |
| Student > Master | 6 | 11% |
| Researcher | 5 | 9% |
| Other | 6 | 11% |
| Unknown | 15 | 28% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 11 | 20% |
| Medicine and Dentistry | 9 | 17% |
| Agricultural and Biological Sciences | 6 | 11% |
| Immunology and Microbiology | 4 | 7% |
| Pharmacology, Toxicology and Pharmaceutical Science | 3 | 6% |
| Other | 2 | 4% |
| Unknown | 19 | 35% |
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 19 August 2015.
All research outputs
#20,288,585
of 22,824,164 outputs
Outputs from Inflammation Research
#786
of 956 outputs
Outputs of similar age
#220,966
of 264,090 outputs
Outputs of similar age from Inflammation Research
#14
of 23 outputs
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