HYDROGEN PREVENTS LIPOPOLYSACCHARIDE-INDUCED PULMONARY MICROVASCULAR ENDOTHELIAL CELL INJURY BY INHIBITING STORE-OPERATED Ca 2+ ENTRY REGULATED BY STIM1/ORAI1.
Yuan Li, Hongguang Chen, Ruichen Shu, Xuan Zhang, Guiyue Wang, Yiqing Yin · Shock (Augusta, Ga.) · 2024
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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 vitro, LPS treatment increased the expression levels of STIM1 and Orai1 in PMVECs, while H₂ reversed these changes. The authors concluded that the present study suggested that H₂ treatment alleviates LPS-induced PMVEC dysfunction by inhibiting store-operated Ca 2+ entry mediated by STIM1 and Orai1 in vitro and in vivo. 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 Moreover, the researchers also investigated the role of H₂-rich medium in regulating PMVECs under LPS treatment, which induced injury similar to sepsis in vitro. LPS treatment increased the expression levels of STIM1 and Orai1 in PMVECs, while H₂ reversed these changes.
What the Researchers Studied
The researchers studied Moreover, the researchers also investigated the role of H₂-rich medium in regulating PMVECs under LPS treatment, which induced injury similar to sepsis in vitro. The study used a in vitro cell-culture laboratory experiment.
What Effects Did Molecular Hydrogen Have?
In vitro, LPS treatment increased the expression levels of STIM1 and Orai1 in PMVECs, while H₂ reversed these changes. The authors concluded that the present study suggested that H₂ treatment alleviates LPS-induced PMVEC dysfunction by inhibiting store-operated Ca 2+ entry mediated by STIM1 and Orai1 in vitro and in vivo. The authors' preliminary results indicated that hydrogen gas (H₂ ) treatment significantly alleviates lung injury in sepsis, protects PMVECs from hyperpermeability, and decreases the expression of plasma membrane stromal interaction molecule 1 (STIM1), but the underlying mechanism by which H₂ maintains Ca 2+ homeostasis in endothelial cells in septic models remains unclear.
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 Moreover, the researchers also investigated the role of H₂-rich medium in regulating PMVECs under LPS treatment, which induced injury similar to sepsis 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.