Hydrogen gas alleviates acute ethanol-induced hepatotoxicity in mice via modulating TLR4/9 innate immune signaling and pyroptosis.
Luyao Xu, Wenhai Guo, Jiaying Dai, Ya Cheng, Yun Chen, Wei Liu, Jiean Xu, Wen Su, Xiaodong Zhang, Changjun Wang, Hongzhi Yang, Jinwen Xu, Yaxing Zhang · International immunopharmacology · 2024
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Independent study record
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H2HUBB TAKEAWAY
In mice, intraperitoneal injection of H₂ improved acute ethanol-induced liver injury in mice in a dose dependent manner, as indicated by decreasing serum ALT and AST levels, hepatic TG levels, and increasing lipid export genes (Mttp and Apob) mRNA levels and reducing fatty acid uptake gene (CD36) mRNA levels. 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 mice. Intraperitoneal injection of H₂ improved acute ethanol-induced liver injury in mice in a dose dependent manner, as indicated by decreasing serum ALT and AST levels, hepatic TG levels, and increasing lipid export genes (Mttp and Apob) mRNA levels and reducing fatty acid uptake gene (CD36) mRNA levels.
What the Researchers Studied
The researchers studied mice. The study used a preclinical animal experiment.
What Effects Did Molecular Hydrogen Have?
However, the dose effects and innate immune mechanisms of intraperitoneal injection of H₂ on ALD are limited. Here, the researchers used acute ethanol-induced hepatotoxicity mice models to estimate the actions of intraperitoneal injection of H₂ on ALD. intraperitoneal injection of H₂ improved acute ethanol-induced liver injury in mice in a dose dependent manner, as indicated by decreasing serum ALT and AST levels, hepatic TG levels, and increasing lipid export genes (Mttp and Apob) mRNA levels and reducing fatty acid uptake gene (CD36) mRNA levels. The authors concluded that mechanistically, H₂ inhibited hepatic oxidative stress as indicated by reducing reactive oxygen species (ROS), 3-NT, and MDA levels in the liver, while increasing hepatic GSH levels; inhibited the overactived TLR4/9-NF-κB-TNF-α/IL-1β/IL-18 innate immune signaling; suppressed the canonical Caspase-1-GSDMD pyroptosis signaling, and the non-canonical pyroptosis signaling, such as Caspase-11-GSDMD, Caspase-8-GSDMD and Caspase-3-GSDME signaling.
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 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.