Hydrogen Research Study
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Laboratory or cellular evidenceLaboratory StudyOther or not reported

Molecular hydrogen attenuates sepsis-induced neuroinflammation through regulation of microglia polarization through an mTOR-autophagy-dependent pathway.

Xinqi Zhuang, Yang Yu, Yi Jiang, Sen Zhao, Yuzun Wang, Lin Su, Keliang Xie, Yonghao Yu, Yuechun Lu, Guoyi Lv · International immunopharmacology · 2020

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 Research Library branded molecular hydrogen research image
Primary topic Sepsis and Critical Care
Evidence type Laboratory or cellular evidence
Publication type Laboratory Study
Hydrogen method Other or not reported

H2HUBB TAKEAWAY

In MHY1485, an mTOR activator, abolished the protective effects of hydrogen in vitro, hydrogen treatment decreased the ratio of p-mTOR/mTOR and the expression of p62 and increased the ratio of p-AMPK/AMPK, LC3II/LC3I and the expression of TREM-2 and Beclin-1 in LPS-treated BV-2 cells. 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 molecular hydrogen affected the outcomes measured in MHY1485, an mTOR activator, abolished the protective effects of hydrogen in vitro. Hydrogen treatment decreased the ratio of p-mTOR/mTOR and the expression of p62 and increased the ratio of p-AMPK/AMPK, LC3II/LC3I and the expression of TREM-2 and Beclin-1 in LPS-treated BV-2 cells.

What the Researchers Studied

The researchers studied MHY1485, an mTOR activator, abolished the protective effects of hydrogen in vitro. The study used a in vitro cell-culture laboratory experiment.

What Effects Did Molecular Hydrogen Have?

Hydrogen treatment decreased the ratio of p-mTOR/mTOR and the expression of p62 and increased the ratio of p-AMPK/AMPK, LC3II/LC3I and the expression of TREM-2 and Beclin-1 in LPS-treated BV-2 cells. This research aimed to determine whether hydrogen alleviates SAE by regulating microglia polarization and whether it is mediated by the mammalian target of rapamycin (mTOR)-autophagy pathway. Taken together, these results demonstrated that hydrogen attenuated sepsis-induced neuroinflammation by modulating microglia polarization, which was mediated by the mTOR-autophagy signaling pathway.

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 MHY1485, an mTOR activator, abolished the protective effects of hydrogen in vitro. The study used a in vitro cell-culture laboratory 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.