[Effects of hydrogen-rich medium on lipopolysaccharide-induced intestinal epithelial barrier dysfunction of human colon carcinoma cells].
Tao Yang, Keliang Xie, Hongguang Chen, Hongtao Zhang, Yang Yu, Guolin Wang, Yonghao Yu · Zhonghua wei zhong bing ji jiu yi xue · 2016
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Independent study record
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H2HUBB TAKEAWAY
In a laboratory model, hydrogen-rich medium can effectively attenuate LPS-induced dysfunction of intestinal epithelial barrier in human Caco2 cells by ameliorating cell viability as well as regulating claudin-1 and occludin expression and structure. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.
What the Researchers Tested
To investigate the effects of hydrogen-rich medium on lipopolysaccharide (LPS)-induced intestinal epithelial barrier dysfunction of human intestinal epithelial (Caco2) cells.
How Molecular Hydrogen Was Used
These cells were randomly divided into four groups: control group (group A), hydrogen-rich medium group (group B), LPS group (group C) and LPS + hydrogen-rich medium group (group D). Cells were cultured with normal medium in group A and group C or with hydrogen-rich medium in group B and group D. Cell viability and cytotoxicity were assessed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and lactate dehydrogenase (LDH) release assay, respectively, after incubation for 24 hours.
What Molecular Hydrogen Changed
Compared with group A, it was shown that TEER was time-dependently decreased in groups C and D after 6 hours. Compared with group C, TEER in group D was increased after 6 hours.
H₂ Mechanisms / Biological Findings
The source material reviewed did not establish a specific molecular hydrogen mechanism for the reported findings.
Authors’ Conclusion
The authors concluded that hydrogen-rich medium can effectively attenuate LPS-induced dysfunction of intestinal epithelial barrier in human Caco2 cells by ameliorating cell viability as well as regulating claudin-1 and occludin expression and structure.