Hydrogenology
Source-linked study record

Hydrogen-rich saline inhibits tobacco smoke-induced chronic obstructive pulmonary disease by alleviating airway inflammation and mucus hypersecretion in rats

Liu Z, Geng W, Jiang C, Zhao S, Liu Y, Zhang Y, Qin S, Li C, Zhang X, Si Y. · Experimental Biology and Medicine. 2017;242(15):1534-1541.

PreclinicalOther formsPublished 2017Source 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

Twenty-four male Sprague-Dawley rats; COPD was modelled by tobacco-smoke exposure for 12 weeks.

Intervention and dose

H₂-rich saline 10 mL/kg intraperitoneally twice daily, 30 minutes before smoke exposure, during weeks 9-12. · Hydrogen was dissolved in saline for two hours at 0.4 MPa; solution was freshly prepared weekly, gamma-sterilized, stored at 4°C and maintained above 0.6 mM.

Duration

Tobacco smoke twice daily for 12 weeks; H₂-rich saline twice daily during the final four weeks.

Reported result

Compared with smoke plus normal saline, H₂-rich saline improved the reported lung-function measures and histology, reduced inflammatory cells, IL-6, IL-8, IL-10, MDA and MUC5AC, and increased AQP5. This was a prevention/attenuation model without an H₂-only healthy group, and the article does not establish reversal of human COPD.

Main limitation

Small male-rat study, surrogate and histological endpoints, prophylactic timing before each smoke exposure, no dose-response assessment and no human participants. Chinese public/provincial/institutional grants funded the work; authors declared no conflicts of interest.

Evidence and classification

What kind of evidence is this?

Evidence type

Preclinical

Reported design

Randomized three-group controlled rat study

Research topic

Respiratory health

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

Twenty-four male Sprague-Dawley rats; COPD was modelled by tobacco-smoke exposure for 12 weeks.

Sample

24 rats randomized to control, tobacco-smoke and tobacco-smoke plus H₂-rich saline groups, n=8 each.

Duration

Tobacco smoke twice daily for 12 weeks; H₂-rich saline twice daily during the final four weeks.

Intervention

H₂-rich saline 10 mL/kg intraperitoneally twice daily, 30 minutes before smoke exposure, during weeks 9-12.

Hydrogen form

H₂ dissolved in normal saline — H₂ only, not Brown's gas.

Dose or H₂ specification

Hydrogen was dissolved in saline for two hours at 0.4 MPa; solution was freshly prepared weekly, gamma-sterilized, stored at 4°C and maintained above 0.6 mM.

Comparator

Air-exposed controls and tobacco-smoke rats receiving equal-volume normal saline injections.

Reported, not endorsed

Outcomes and reported result

Outcomes measured

Lung resistance and compliance, FEV0.1/FVC, lung histology, inflammatory cells and cytokines, MDA, airway MUC5AC and lung AQP5.

Reported result

Compared with smoke plus normal saline, H₂-rich saline improved the reported lung-function measures and histology, reduced inflammatory cells, IL-6, IL-8, IL-10, MDA and MUC5AC, and increased AQP5. This was a prevention/attenuation model without an H₂-only healthy group, and the article does not establish reversal of human COPD.

Extraction completeness

The complete free PMC article was checked for randomization, groups, H₂ preparation and concentration, dose and timing, result tables and figures, funding and conflict declaration.

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

Interpretation limits

Limitations and applicability

Main methodological cautions

Small male-rat study, surrogate and histological endpoints, prophylactic timing before each smoke exposure, no dose-response assessment and no human participants. Chinese public/provincial/institutional grants funded the work; authors declared no conflicts of interest.

Applies directly to

Tobacco-smoke COPD model in male rats; it does not establish a treatment or dose for people with COPD.

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: 28795606 · DOI: 10.1177/1535370217725249

Publisher access

Free full article in PubMed Central; the journal landing page may otherwise show restricted access.

Extraction basis

Complete PMC article and PubMed metadata; full-text extraction checked 9 August 2026.

Last reviewed

10 August 2026

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