Hydrogen-rich saline protects against mitochondrial dysfunction and apoptosis in mice with obstructive jaundice.
Qu Liu, Bao-Shan Li, Yu-Jiao Song, Ming-Gen Hu, Jian-Yue Lu, Ang Gao, Xue-Jun Sun, Xi-Ming Guo, Rong Liu · Molecular medicine reports · 2016
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Independent study record
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H2HUBB TAKEAWAY
In male C57BL/6 mice, treatment with HS reduced the levels of these markers and alleviated morphological defects in the mitochondria following injury. These preclinical findings add evidence supporting molecular hydrogen's therapeutic potential within the outcomes and biological pathways measured in this model.
What the Findings Mean
H2HUBB reviewed how molecular hydrogen affected the outcomes measured in male C57BL/6 mice. Treatment with HS reduced the levels of these markers and alleviated morphological defects in the mitochondria following injury.
What the Researchers Studied
The researchers studied male C57BL/6 mice. The study used a preclinical animal experiment. The comparison condition was control condition or baseline measurements.
What Effects Did Molecular Hydrogen Have?
ROS are able to trigger the opening of mitochondrial permeability transition (MPT) pores in the mitochondrial inner membrane, which nonspecifically transport solutes up to a molecular mass of Hydrogen-rich saline protects against mitochondrial dysfunction and apoptosis in mice with obstructive jaundice QU LIU1,2*, BAO-SHAN LI2*, YU-JIAO SONG3*, MING-GEN HU1, JIAN-YUE LU2, ANG GAO2, XUE-JUN SUN4, XI-MING GUO3 and RONG LIU1 1Department of Surgical Oncology, The General Hospital of Chinese People's Liberation Army, Beijing 100853; 2Department of General Surgery, People's Liberation Army No. China E‑mail: guoxim@163.com *Contributed equally Abbreviations: OJ, obstructive jaundice; ROS, reactive oxygen species; MPT, mitochondrial permeability transition; H₂, hydrogen; HS, hydrogen -rich saline; BDL, bile duct ligation; mMDA, mitochondrial malondialdehyde; mGSH, mitochondrial glutathione; mGSSG, mitochondrial glutathione disulfide; mSOD, mitochondrial superoxide dismutase; mCAT, mitochondrial catalase; mGpx, mitochondrial glutathione peroxidase; TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling; HBSS, Hank's balanced salt solution; PBS, phosphate -buffered saline; TEM, transmission electron microscopy; SOD2, superoxide dismutase; CsA, cyclosporin A; MPT, mitochondrial potential transition; RCR, respiratory control ratio; ADP /O, oxidative phosphorylation; ANOVA, analysis of variance; NS, normal saline; MMP, mitochondrial membrane potential Key words: hydrogen-rich saline, obstructive jaundice, mitochondrial oxidative stress, mitochondrial injury, apoptosis LIU et al: HYDROGEN-RICH SALINE PROTECTS AGAINST MITOCHONDRIAL INJURY IN BDL MICE 3589 1,500 Da (6). Treatment with HS reduced the levels of these markers and alleviated morphological defects in the mitochondria following injury. The authors concluded that in conclusion, HS attenuates mitochondrial oxidative stress and dysfunction, and inhibits mitochondrial-mediated apoptosis in the livers of BDL mice.
Why These Findings Matter
These preclinical findings add evidence supporting molecular hydrogen's therapeutic potential within the outcomes and biological pathways measured in this model.
How Strong Is This Evidence?
This is preclinical animal evidence from a preclinical animal experiment. It is most informative for the disease model, mechanisms, biomarkers, and outcomes directly measured in the study.
Technical Study Details
H2HUBB classifies this publication as animal study with preclinical animal evidence. The research population or model was male C57BL/6 mice. The study used a preclinical animal experiment.
Limitations and Safety
No separate limitations or safety findings were identified in the source text available to H2HUBB.
Original Study and H2HUBB Research Context
H2HUBB presents this source-grounded research record as one contribution to the broader molecular-hydrogen evidence base. The original scholarly source is available at https://www.spandidos-publications.com/10.3892/mmr.2016.4954/download.