水素と埋没針療法の併用が外傷性脳損傷においてSTINGシグナル経路を介したNLRP3インフラマソーム活性化を抑制する機序の解明
Using a controlled cortical impact (CCI) mouse model of traumatic brain injury (TBI), this study examined the effects of molecular hydrogen (H), needle-embedding therapy (NET), and their combination (H+NET). Assessments included neurological severity scoring, Nissl staining, TUNEL apoptosis assay, ELISA for ATP, adenosine, and inflammatory cytokines, qRT-PCR for inflammatory gene expression, and immunofluorescence and Western blot for NLRP3 inflammasome and STING pathway proteins. CCI induction elevated microglial activation, NLRP3 inflammasome activity, and STING signaling. H alone or NET alone partially reduced brain edema and neuroinflammation. However, the H+NET combination produced significantly greater suppression of NLRP3 inflammasome activation and STING pathway signaling, accompanied by more pronounced reductions in brain water content and inflammatory cytokine levels compared with either monotherapy.
The combination of hydrogen and needle-embedding therapy suppresses the STING signaling pathway, thereby inhibiting downstream NLRP3 inflammasome activation, reducing microglial-mediated neuroinflammation, and alleviating cerebral edema in TBI.
This study combines multiple delivery routes. As a general principle, the most efficient route for routine hydrogen intake is inhalation. Inhalation carries explosion risk (empirical LFL of 10%; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/40187069