Effects of Low Concentration Hydrogen Inhalation on Asthma and Sleep Function in Mice
Zhao Yue; Wei Lu; Zhang Xue-wei; Zhu Li; Du Jun-rong · Journal of Sichuan University (Medical Sciences). 2020;51(2):219–224.
Study at a glance
In mice, low-concentration hydrogen inhalation changed some inflammation measurements in an asthma model. A separate experiment found changes in pentobarbital-induced sedation, while one sedation-incidence comparison was not significant. These findings do not establish treatment for human asthma or sleep problems.
Preclinical
Separate BALB/c ovalbumin-asthma and ICR pentobarbital-induced sedation experiments; mice of both sexes, body mass 20 ± 2 g. No human participants.
QMK-98500Y generator hydrogen mixed with air. Asthma exposure: 30 minutes daily for 7 days during ovalbumin challenge. Separate sedation experiments: 30 minutes twice daily for 1, 3 or 5 days before pentobarbital challenge. · 24–26 mL H₂ per litre of gas, equivalent to 2.4–2.6% by volume. This is concentration, not gas flow.
Asthma: 30 minutes/day for 7 days. Separate sedation assays: 30 minutes twice daily for 1, 3 or 5 days, followed by pentobarbital challenge.
Versus ovalbumin + air, IL-4/IL-13 decreased and IFN-γ increased (P < 0.05); GSH and SOD increased, while MDA change was nonsignificant. Histology appeared less damaged. In separate sedation experiments, hydrogen shortened pentobarbital-induced latency and prolonged duration versus air, with weaker effects than diazepam. Subthreshold incidence: air 2/10; hydrogen day 1 and day 5 each 8/10 (P < 0.01 versus air); day 3 was 6/10 and nonsignificant; diazepam 10/10. A monotonic exposure-duration response was not established.
Animal models only. Pentobarbital-induced loss of righting reflex is not natural sleep or evidence for treating insomnia. Asthma and sedation used separate mouse strains; sleep improvement in asthmatic mice was not demonstrated. No objective airway-resistance test, blinded assessment, prespecified primary endpoint or independent exposure validation was reported. Multiple exploratory outcomes and incomplete assay-flow accounting limit interpretation.
What kind of evidence is this?
Preclinical
Randomized animal experiments; blinding, sample-size calculation and prespecified primary endpoint not reported.
吸入低浓度氢气对小鼠哮喘和睡眠功能的影响
Respiratory health
Inhaled H₂
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.
Methods
Separate BALB/c ovalbumin-asthma and ICR pentobarbital-induced sedation experiments; mice of both sexes, body mass 20 ± 2 g. No human participants.
Asthma experiment: 35 mice randomized by body mass to 3 groups, 11–12 per group. Sedation assays: 5 groups of 10 per group. Whether animals were reused between pentobarbital-threshold assays is unclear, so no combined animal total is asserted. Assay-specific attrition was not reported.
Asthma: 30 minutes/day for 7 days. Separate sedation assays: 30 minutes twice daily for 1, 3 or 5 days, followed by pentobarbital challenge.
QMK-98500Y generator hydrogen mixed with air. Asthma exposure: 30 minutes daily for 7 days during ovalbumin challenge. Separate sedation experiments: 30 minutes twice daily for 1, 3 or 5 days before pentobarbital challenge.
Low-concentration H₂ mixed with air, not a drinking-water intervention.
24–26 mL H₂ per litre of gas, equivalent to 2.4–2.6% by volume. This is concentration, not gas flow.
Gas flow and achieved tissue dose were not reported.
Hydrogen was mixed with air; a separately measured inspired oxygen fraction was not reported.
Asthma: normal/PBS and ovalbumin + air groups. Sedation: air + pentobarbital; positive comparator diazepam 2.5 mg/kg on day 5. Pentobarbital was 60 mg/kg for suprathreshold or 40 mg/kg for subthreshold assays.
Outcomes and reported result
BALF IL-4, IL-13 and IFN-γ; lung MDA, GSH, SOD and histology. Separate pentobarbital-induced loss-of-righting-reflex latency, duration and incidence; these are not natural-sleep architecture measurements.
Versus ovalbumin + air, IL-4/IL-13 decreased and IFN-γ increased (P < 0.05); GSH and SOD increased, while MDA change was nonsignificant. Histology appeared less damaged. In separate sedation experiments, hydrogen shortened pentobarbital-induced latency and prolonged duration versus air, with weaker effects than diazepam. Subthreshold incidence: air 2/10; hydrogen day 1 and day 5 each 8/10 (P < 0.01 versus air); day 3 was 6/10 and nonsignificant; diazepam 10/10. A monotonic exposure-duration response was not established.
The available main full text was reviewed for methods, results, limitations and declarations. Uncertainties, supplementary-source limits and conflicting findings are stated in this record.
No dedicated systematic adverse-event assessment was located. General safety statements in the article do not establish human or consumer-device safety.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
Animal models only. Pentobarbital-induced loss of righting reflex is not natural sleep or evidence for treating insomnia. Asthma and sedation used separate mouse strains; sleep improvement in asthmatic mice was not demonstrated. No objective airway-resistance test, blinded assessment, prespecified primary endpoint or independent exposure validation was reported. Multiple exploratory outcomes and incomplete assay-flow accounting limit interpretation.
Only the reported mouse asthma and drug-induced sedation experiments; no human asthma or insomnia outcome.
No funding declaration was located in the complete six-page article.
No dedicated conflict statement was located. The device manufacturer is named as a supplier; absence of a conflict is not inferred.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 32220191 · DOI: 10.12182/20200360103
Complete six-page Chinese-language publisher article, pages 219–224, including the English abstract and all four figure legends.
AI-assisted editorial review of the available main full text, 29 October 2026. No independent clinical or statistical assessment has been performed.
Complete article, pages 219–224; Materials and methods 1.1–1.5; Results 2.1–2.2 and all four figure legends; Discussion and references.
AI-assisted editorial review of the available main full text, 29 October 2026. Complete six-page Chinese-language publisher article, pages 219–224, including the English abstract and all four figure legends.
The article states conformity with GB/T 35892-2018 animal-welfare guidance; a named ethics committee and approval number were not located.
29 October 2026
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