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Hydrogen-rich saline promotes microglia M2 polarization and complement-mediated synapse loss to restore behavioral deficits following hypoxia-ischemic injury in neonatal mice via AMPK activation

Chu X et al. · J Neuroinflammation. 2019;16:104.

PreclinicalOther formsPublished 2019Source checked
Study record, not medical adviceThis record reports what the source states. It is not medical advice and does not establish that molecular hydrogen is effective, safe or appropriate for any person.
Quick summary

Study at a glance

Evidence type

Preclinical

Population or model

Postnatal-day-7 mouse pups with Rice-Vannucci hypoxia-ischemia injury and cultured BV-2 cells

Intervention and dose

Hydrogen-rich saline 5 mL/kg intraperitoneally on days 1, 2 and 3 after hypoxia-ischemia, with additional AMPK-inhibitor experiments · >0.6 mM dissolved H₂; saline was prepared for 12 hours at 0.4 MPa and concentration was checked with a dissolved-H₂ meter.

Duration

Treatment on post-injury days 1–3, with acute tissue and later behavioral and synaptic assessments

Reported result

The article reports less neuroinflammation, improved behavioral and synaptic measures and changes consistent with AMPK activation; an AMPK inhibitor reversed several reported effects.

Main limitation

Complex neonatal mouse and cell study with multiple mechanistic groups and outcomes. It does not establish treatment benefit after human neonatal hypoxic-ischemic injury.

Evidence and classification

What kind of evidence is this?

Evidence type

Preclinical

Reported design

Controlled neonatal-mouse hypoxia-ischemia experiment plus BV-2 microglial-cell experiments

Research topic

Other neurological conditions

Administration form

Other forms

Information not yet classified

Some editorial classification fields are still pending. The source-reported outcomes and result are shown below; Hydrogenology does not infer a positive or negative signal from prose automatically.

Reported in the source

Methods

Population or model

Postnatal-day-7 mouse pups with Rice-Vannucci hypoxia-ischemia injury and cultured BV-2 cells

Sample

Multiple cohorts: principal tissue assays n=4–6/group and behavioral cohorts n=10/group; the article does not present a single total animal count

Duration

Treatment on post-injury days 1–3, with acute tissue and later behavioral and synaptic assessments

Intervention

Hydrogen-rich saline 5 mL/kg intraperitoneally on days 1, 2 and 3 after hypoxia-ischemia, with additional AMPK-inhibitor experiments

Hydrogen form

H₂ dissolved in saline or culture medium — H₂ only, not Brown’s gas and not inhalation.

Dose or H₂ specification

>0.6 mM dissolved H₂; saline was prepared for 12 hours at 0.4 MPa and concentration was checked with a dissolved-H₂ meter.

Comparator

Hypoxia-ischemia without H₂, sham controls and AMPK-inhibitor comparison groups

Reported, not endorsed

Outcomes and reported result

Outcomes measured

Inflammatory-cell accumulation, microglial polarization, AMPK and NF-κB, neurological behavior, synaptic proteins and complement components

Reported result

The article reports less neuroinflammation, improved behavioral and synaptic measures and changes consistent with AMPK activation; an AMPK inhibitor reversed several reported effects.

Extraction completeness

The complete open-access article and supplementary cohort descriptions were checked for dose, concentration, allocation by assay, schedules, positive and null outcomes, funding and conflicts.

A reported association, difference or mechanism is not automatically a clinical benefit.

Interpretation limits

Limitations and applicability

Main methodological cautions

Complex neonatal mouse and cell study with multiple mechanistic groups and outcomes. It does not establish treatment benefit after human neonatal hypoxic-ischemic injury.

Applies directly to

Neonatal hypoxia-ischemia in mice and cultured microglia.

No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.

Sources and status

Sources and record status

Identifiers

PMID: 31103039 · DOI: 10.1186/s12974-019-1488-2

Publisher access

Open-access full text is available through PMC and the publisher.

Extraction basis

Open-access publisher/PMC full text and PubMed record.

Last reviewed

10 August 2026

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