Hydrogen Mitigated Doxorubicin-Induced Liver Injury via Nrf2/HO-1 Pathway Activation.
Meng-Fan Sun, Ji-Xian Song, Miao Tang, Bo-Han Yu, Yao Xiao, Yu-Hui Gao, Zi-Xuan Yao, Ke-Ying An, Zhen-Qun Zhang, Yong-Qing Shen, Ya-Shuo Zhao · International journal of molecular sciences · 2026
Research-use notice
Independent study record
Each H2HUBB study page organizes source-linked research details for educational use. Interpretation should remain proportional to the study design, population, controls, and limitations.
H2HUBB TAKEAWAY
In Hydrogen was found to suppress apoptosis, reduce oxidative stress levels, and ameliorate inflammatory responses in the liver tissue of DOX mice, hydrogen treatment significantly mitigated DOX-induced liver damage and inhibited hepatocyte fibrosis. The authors concluded that these results suggest that hydrogen may mitigate DOX-induced liver injury by activating the Nrf2/HO-1 signaling pathway, consequently diminishing oxidative stress and inflammatory responses. These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
What the Findings Mean
H2HUBB reviewed how hydrogen-rich medium affected the outcomes measured in Hydrogen was found to suppress apoptosis, reduce oxidative stress levels, and ameliorate inflammatory responses in the liver tissue of DOX mice. Hydrogen treatment significantly mitigated DOX-induced liver damage and inhibited hepatocyte fibrosis.
What the Researchers Studied
The researchers studied Hydrogen was found to suppress apoptosis, reduce oxidative stress levels, and ameliorate inflammatory responses in the liver tissue of DOX mice. The study used a in vitro cell-culture laboratory experiment. The comparison condition was control condition or baseline measurements.
What Effects Did Molecular Hydrogen Have?
A total of 40 C57BL/6N mice were randomly assigned to four groups: the control group (Con), the DOX group, the DOX combined with hydrogen-rich saline solution (DOX+hydrogen-rich saline) group, and the control combined with hydrogen-rich saline solution (Con+hydrogen-rich saline) group. In summary, hydrogen was dissolved in normal saline for six hours at 0.4 Megapascals (MPa) to achieve a supersaturated state using a hydrogen production apparatus. A needle-type hydrogen sensor (Unisense A/S) was employed to monitor the hydrogen concentration [ 27, 40 ]. Hydrogen treatment significantly mitigated DOX-induced liver damage and inhibited hepatocyte fibrosis. The authors concluded that these results suggest that hydrogen may mitigate DOX-induced liver injury by activating the Nrf2/HO-1 signaling pathway, consequently diminishing oxidative stress and inflammatory responses. Hydrogen was found to suppress apoptosis, reduce oxidative stress levels, and ameliorate inflammatory responses in the liver tissue of DOX mice.
Why These Findings Matter
These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
How Strong Is This Evidence?
This is laboratory evidence from a in vitro cell-culture laboratory experiment. It is most informative for the biological mechanisms, cellular responses, or biochemical outcomes directly measured.
Technical Study Details
H2HUBB classifies this publication as laboratory study with laboratory or cellular evidence. The research population or model was Hydrogen was found to suppress apoptosis, reduce oxidative stress levels, and ameliorate inflammatory responses in the liver tissue of DOX mice. The study used a in vitro cell-culture laboratory experiment. The hydrogen delivery method was hydrogen-rich medium.
Limitations and Safety
No separate limitations or safety findings were identified in the current-study 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.