Hydrogen Particles Heal Esophageal Wounds and Boost Cell Movement
- Authors
- Yoshiharu Tanaka, Qiang Li, Nobuhiko Miwa
- Journal
- Medical Gas Research
- Year
- 2018
- DOI
- 10.4103/2045-9912.235128
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Esophageal Injuries
- Body System
- Digestive System
TL;DR
Adding hydrogen to silica particles can help skin cells move and repair wounds, but too much may cause the cells to self-destruct.
Key Finding
Hydrogen-occluding silica microparticles promoted wound repair and cell migration in esophageal cells at low concentrations (10-100 ppm), but induced excessive cell death at higher concentrations (>300 ppm).
Summary
Researchers tested hydrogen-releasing silica particles on human esophageal cells in a laboratory dish to see if they could help cells repair wounds and move across damaged areas. At low concentrations (10-100 parts per million), the particles promoted cell migration and wound healing, likely by reducing harmful molecules called free radicals. However, at higher concentrations (above 300 ppm), the particles triggered excessive cell death, suggesting there's a narrow range where they might be helpful without causing damage.
Practical Takeaway
This laboratory study suggests hydrogen-releasing particles may have potential for treating esophageal injuries, but only within a specific dose range. Because this is early-stage cell culture research with no human testing, it's too preliminary to draw conclusions about whether hydrogen water or similar products would have similar effects in people. Much more research, including animal and human studies, would be needed before any clinical applications could be considered.
Abstract
Many conventional studies on molecular hydrogen have not examined cell migration ability and the relationship between apoptosis and the cytoskeleton. Here we investigated the influence of hydrogen-occluding silica microparticles (H2-silica) on cell migration motility and changes of the cytoskeleton (F-actin) in normal human esophageal epithelial cells (HEEpiCs). As the results, cell migration was promoted, and formation of microvilli was activated in the 100 ppm (low concentration) scratched group. After performing a wound healing assay, cells exhibited migration after 48 hours and 72 hours for both 10 ppm and 100 ppm groups, suggesting that the wound-repairing effects could be attributed to the antioxidant ability of H2-silica. In scratched groups, high levels of activated caspase-3 were relatively expressed and presented a tendency to increase the observed Bax/Bcl-2 ratio at more than 300 ppm groups. The above-mentioned results show that H2-silica induced apoptosis in HEEpiCs, especially in the scratched cells. Toxicity may cause an exaggerated apoptosis. Furthermore, since the ratio of fascin/tubulin in the 100, 300, and 600 ppm groups tended to increase in both the scratched and the non-scratched control groups, H2-silica was thought to be able to promote fascin action on normal cells and may be have a proliferative effect.