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Molecular hydrogen regulates the expression of miR-9, miR-21 and miR-199 in LPS-activated retinal microglia cells.

LPS活性化網膜ミクログリア細胞におけるmiR-9・miR-21・miR-199発現に対する水素分子の調節作用

in vitro study in vitro positive

Abstract

Retinal microglia cells were stimulated with lipopolysaccharide (LPS) and subsequently exposed to hydrogen-saturated medium or control medium. qRT-PCR analysis revealed that hydrogen exposure led to marked decreases in miR-9 and miR-21 levels, while miR-199 expression was elevated. Western blotting of LPS-induced signaling proteins showed reduced Myd88 and IKK-β levels following hydrogen treatment, along with increased PDCD4 expression; NF-κB levels remained unchanged. These findings suggest that molecular hydrogen modulates inflammatory signaling in retinal microglia through coordinated regulation of specific miRNAs, providing a mechanistic basis for its protective effects against inflammatory injury in retinal tissue.

Mechanism

Molecular hydrogen suppresses miR-9 and miR-21 while upregulating miR-199, resulting in reduced Myd88 and IKK-β expression and increased PDCD4, thereby attenuating upstream NF-κB inflammatory signaling in LPS-activated retinal microglia.

Bibliographic

Authors
Liu GD, Zhang H, Wang L, Han Q, Zhou SF, Liu P
Journal
Int J Ophthalmol
Year
2013
PMID
23826519
DOI
10.3980/j.issn.2222-3959.2013.03.05
PMC
PMC3693006

Tags

Disease:網膜疾患 Mechanism:アポトーシス抑制 免疫調節 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:

Other papers on the same disease / condition

Cite as: H2 Papers — PMID 23826519. https://h2-papers.org/en/papers/23826519
Source: PubMed PMID 23826519