Inhibition Effect of Hydrogen Water on Cisplatin Induced Hepatocyte Injury via Upregulating NFE2L2/HMOX1 Expression
Wang Han; Chen Jianhua; Song Shili; Hao Zhen; Huo Zhongchao; Li Sha; Li Weixia · Chinese General Practice. 2026;29(29):4288–4294.
Study at a glance
Hydrogen-containing medium reduced some cisplatin-associated injury measurements in a laboratory cell culture. The authors described the cells as normal liver cells, but Cellosaurus identifies the named WRL68 line as a HeLa derivative. These results do not establish protection of normal liver cells or people receiving chemotherapy.
Preclinical
WRL68 cell culture, described by the authors as normal liver cells. The named line is classified as a problematic HeLa derivative by Cellosaurus; the specific stock used was not independently genotyped. No patients or verified normal hepatocytes.
CHD-1 apparatus produced hydrogen water measured by headspace gas chromatography. RPMI 1640 medium was prepared with hydrogen water and 10% fetal bovine serum. Screening concentrations were 0.6, 0.9 and 1.2 mg/L. Selected exposure: 0.6 mg/L for 24 hours before 3 mg/L cisplatin for 24 hours; 48 hours total. · Selected dissolved H₂ concentration 0.6 mg/L for 24-hour pretreatment, followed by 3 mg/L cisplatin for 24 hours. Hydrogen retention during incubation was not measured over time.
24-hour pretreatment followed by 24-hour cisplatin exposure; 48 hours total.
Cisplatin-only viability was 59.93 ± 2.89%; hydrogen pretreatment at 0.6, 0.9 and 1.2 mg/L gave 77.50 ± 3.67%, 72.28 ± 5.94% and 74.15 ± 4.43% respectively (each P < 0.05 versus cisplatin). Hydrogen alone did not significantly change viability versus control. Apoptosis in the four conditions was 2.49 ± 0.38% control, 32.90 ± 1.97% cisplatin, 2.67 ± 0.60% hydrogen alone and 23.15 ± 1.19% hydrogen + cisplatin. Pretreatment reduced ROS from 6.52 ± 0.99 to 4.00 ± 0.40 relative units and partially restored mitochondrial membrane potential. NFE2L2/HMOX1 protein/mRNA expression increased versus cisplatin, but inhibition or knockdown was not used to establish pathway causality. One-way ANOVA/Tukey comparisons used P < 0.05; exact pairwise P values and confidence intervals were not provided.
One cell line, n = 3 and unclear biological/technical replicate independence. Pretreatment is not treatment of established clinical injury. No animal/patient outcomes, pharmacokinetics, chemotherapy antitumor response or clinical safety were assessed. Hydrogen decay, medium pH and other preparation properties were not fully controlled/reported. Expression associations do not demonstrate causal NFE2L2/HMOX1 mediation. Multiple outcomes and in-study dose selection limit interpretation.
What kind of evidence is this?
Preclinical
In vitro dose-screening and four-condition cisplatin-injury experiment; no prespecified primary outcome, randomization or blinded analysis reported.
氢水通过上调核因子红细胞2相关因子2/血红素加氧酶1表达抑制顺铂致肝细胞损伤作用研究
Published online 2 September 2026; journal issue 15 October 2026. The year 2024 in the DOI does not establish the publication year.
Liver health
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.
Methods
WRL68 cell culture, described by the authors as normal liver cells. The named line is classified as a problematic HeLa derivative by Cellosaurus; the specific stock used was not independently genotyped. No patients or verified normal hepatocytes.
Tables 2–5 report n = 3; the pilot method specifies 3 replicate wells per condition. Biological versus technical replicate independence is unclear. No patient or animal sample.
24-hour pretreatment followed by 24-hour cisplatin exposure; 48 hours total.
CHD-1 apparatus produced hydrogen water measured by headspace gas chromatography. RPMI 1640 medium was prepared with hydrogen water and 10% fetal bovine serum. Screening concentrations were 0.6, 0.9 and 1.2 mg/L. Selected exposure: 0.6 mg/L for 24 hours before 3 mg/L cisplatin for 24 hours; 48 hours total.
Molecular hydrogen dissolved in cell-culture medium; neither oral drinking water nor gas inhalation.
Selected dissolved H₂ concentration 0.6 mg/L for 24-hour pretreatment, followed by 3 mg/L cisplatin for 24 hours. Hydrogen retention during incubation was not measured over time.
Standard medium for 48 hours; standard medium for 24 hours then cisplatin for 24 hours; hydrogen medium for 48 hours; hydrogen medium for 24 hours then cisplatin for 24 hours.
Outcomes and reported result
CCK-8 viability, Annexin V/PI apoptosis, mitochondrial membrane potential, ROS, NFE2L2/HMOX1 protein and mRNA. Screening and dose selection belonged to the same experimental program.
Cisplatin-only viability was 59.93 ± 2.89%; hydrogen pretreatment at 0.6, 0.9 and 1.2 mg/L gave 77.50 ± 3.67%, 72.28 ± 5.94% and 74.15 ± 4.43% respectively (each P < 0.05 versus cisplatin). Hydrogen alone did not significantly change viability versus control. Apoptosis in the four conditions was 2.49 ± 0.38% control, 32.90 ± 1.97% cisplatin, 2.67 ± 0.60% hydrogen alone and 23.15 ± 1.19% hydrogen + cisplatin. Pretreatment reduced ROS from 6.52 ± 0.99 to 4.00 ± 0.40 relative units and partially restored mitochondrial membrane potential. NFE2L2/HMOX1 protein/mRNA expression increased versus cisplatin, but inhibition or knockdown was not used to establish pathway causality. One-way ANOVA/Tukey comparisons used P < 0.05; exact pairwise P values and confidence intervals were not provided.
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 clinical adverse-event assessment; cell-culture viability cannot establish safety during chemotherapy.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
One cell line, n = 3 and unclear biological/technical replicate independence. Pretreatment is not treatment of established clinical injury. No animal/patient outcomes, pharmacokinetics, chemotherapy antitumor response or clinical safety were assessed. Hydrogen decay, medium pH and other preparation properties were not fully controlled/reported. Expression associations do not demonstrate causal NFE2L2/HMOX1 mediation. Multiple outcomes and in-study dose selection limit interpretation.
Preclinical observations in the named WRL68 culture only; no verified normal-hepatocyte or clinical liver-protection conclusion.
Hebei Key R&D 223777128D; Handan Science and Technology 23422083045.
Authors declare no conflicts. Two authors were affiliated with the Hydrogen Production Equipment Engineering Department, 718th Research Institute of CSIC; this is not independent device testing.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
Source ID: doi-10.12114-j.issn.1007-9572.2024.0093 · DOI: 10.12114/j.issn.1007-9572.2024.0093
Complete Chinese-language publisher article in rich HTML, including all five tables, discussion and declarations.
AI-assisted editorial review of the available main full text, 29 October 2026. No independent clinical or statistical assessment has been performed.
Introduction; Materials and methods 1.1–1.5, including 1.4.1–1.4.7; Results 2.1–2.5 and Tables 1–5; Discussion; funding and conflict declaration.
AI-assisted editorial review of the available main full text, 29 October 2026. Complete Chinese-language publisher article in rich HTML, including all five tables, discussion and declarations.
No preregistered primary-outcome hierarchy was reported.
29 October 2026
Help people check the facts before they buy.
Hydrogenology keeps 692 source-checked records accessible without advertising or product promotion.
Help us correct the recordReport a discrepancy
Send the exact difference between this page and the linked source. The study reference is attached automatically.