日本語View as Markdown

Molecular hydrogen suppresses Porphyromonas gingivalis lipopolysaccharide-induced increases in interleukin-1 alpha and interleukin-6 secretion in human gingival cells.

分子状水素はPorphyromonas gingivalis LPS誘発性のIL-1αおよびIL-6分泌増加をヒト歯肉細胞において抑制する

in vitro study in vitro positive

Abstract

Using a human gingival cell model of periodontitis, this study investigated how molecular hydrogen (H2) affects the secretion of eight inflammation-related markers induced by Porphyromonas gingivalis lipopolysaccharide (Pg LPS). ELISA measurements revealed that Pg LPS stimulation elevated both interleukin-1 alpha (IL-1α) and interleukin-6 (IL-6) secretion. H2 co-treatment significantly reduced the release of both cytokines without inducing cytotoxicity. These findings indicate that H2 can attenuate the production of key pro-inflammatory cytokines implicated in periodontal disease progression, suggesting a potential role for H2 in modulating gingival inflammatory responses.

Mechanism

H2 is proposed to act as a gaseous antioxidant that reduces oxidative stress in gingival cells, thereby suppressing Pg LPS-driven upregulation of IL-1α and IL-6, two cytokines central to periodontal inflammatory cascades.

Bibliographic

Authors
Saitoh Y, Yonekura N, Matsuoka D, Matsumoto A
Journal
Mol Cell Biochem
Year
2022
PMID
34533646
DOI
10.1007/s11010-021-04262-7

Tags

Mechanism:抗酸化酵素 炎症抑制 酸化ストレス 活性酸素種

Delivery context

This is basic research at the cellular or molecular level. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are not recommended).

Safety notes

This is basic research at the cellular or molecular level. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are not recommended).

See also:

Cite as: H2 Papers — PMID 34533646. https://h2-papers.org/en/papers/34533646
Source: PubMed PMID 34533646