HYDROGEN-RICH MEDIUM AMELIORATES LIPOPOLYSACCHARIDE-INDUCED BARRIER DYSFUNCTION VIA RHOA-MDIA1 SIGNALING IN CACO-2 CELLS.
Tao Yang, Lu Wang, Ruiqiang Sun, Hongguang Chen, Hongtao Zhang, Yang Yu, Yanyan Wang, Guolin Wang, Yonghao Yu, Keliang Xie · Shock (Augusta, Ga.) · 2016
Research-use notice
Independent study record
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H2HUBB TAKEAWAY
In Caco-2 cells were exposed to different concentrations of LPS (1 μg/mL-1 mg/mL), lPS (100 μg/mL) decreased TER and increased fluorescein-isothiocyanate-dextran flux, which were alleviated by H₂-rich medium. 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
Caco-2 cells were exposed to different concentrations of LPS (1 μg/mL-1 mg/mL).
Laboratory Model
Caco-2 cells were exposed to different concentrations of LPS (1 μg/mL-1 mg/mL).
How Molecular Hydrogen Was Used
Hydrogen gas (H₂) can ameliorate multiple organ damage in septic animals. This study was aimed to investigate whether H₂ could modulate lipopolysaccharide (LPS)-stimulated dysfunction of the intestinal barrier and whether RhoA-mDia1 signaling is involved. Also, H₂ down-regulated LPS-induced oxidative stress.
What Molecular Hydrogen Changed
LPS (100 μg/mL) decreased TER and increased fluorescein-isothiocyanate-dextran flux, which were alleviated by H₂-rich medium. H₂ improved the down-regulated expression and redistribution of occludin and E-cadherin caused by LPS. H₂-rich medium increased mDia1 expression, and mDia1 knockdown abolished protections of H₂ on barrier permeability. mDia1 knockdown eliminated H₂-induced benefits for occludin and E-cadherin.
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 H₂ improves LPS-induced hyperpermeability of the intestinal barrier and disruptions of TJ and AJ by moderating RhoA-mDia1 signaling.