General Research
Model: mouse
Hydrogen prevents lipopolysaccharide-induced pulmonary microvascular endothelial cell injury by inhibiting store-operated Ca2+ entry regulated by STIM1/Orai1
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How Hydrogen Helps Protect Your Lungs from Damage
A recent study found that hydrogen can prevent injury to the tiny blood vessels in your lungs by blocking a troublemaker molecule and keeping a special calcium gate closed. This could lead to new treatments for sepsis and other lung conditions. Hydrogen is a powerful tool that can help protect your lungs from damage.
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Publish Year 2023 Country China Rank Positive Journal Shock Primary Topic Lung Secondary TopicSepsis Model Cell Culture Tertiary TopicOxidative Stress Vehicle Medium (Dissolved) pH N/A Application Culture Media Comparison Complement
Background
Methods: We observed the role of H2 on LPS-induced ALI of mice in vivo. The lung wet/dry (W/D) weight ratio, total protein in the bronchoalveolar lavage (BAL) fluid and Evans blue dye (EBD) assay were used to evaluate the pulmonary endothelial barrier damage of LPS-challenged mice. The expression of STIM1 and Orai1 were also detected using epifluorescence microscopy. Moreover, we also investigated the role of H2- rich medium in regulating PMVECs under LPS treatment, which induced injury similar to sepsis in vitro. The expression of STIM1 and Orai1 as well as the Ca2+ concentration in PMVECs were examined.
Methods
Results: In vivo, we found that H2 alleviated ALI of mice through decreasing lung W/D weight ratio, total protein in the BAL fluid and permeability of lung. In addition, H2 also decreased the expression of STIM1 and Orai1 in pulmonary microvascular endothelium. In vitro, LPS treatment increased the expression levels of STIM1 and Orai1 in PMVECs, while H2 reversed these changes. Furthermore, H2 ameliorated Ca2+ influx under sepsis-mimicking conditions. Treatment with the sarco/endoplasmic reticulum Ca2+ adenosine triphosphatase (SERCA) inhibitor, thapsigargin (TG), resulted in a significant reduction in cell viability as well as a reduction in the expression of junctional proteins, including VE-cadherin and occludin. Treatment with the store-operated Ca2+ entry (SOCE) inhibitor, YM-58483 (BTP2), increased the cell viability and expression of junctional proteins. Conclusions: The present study suggested that H2 treatment alleviates LPS-induced PMVEC dysfunction by inhibiting SOCE mediated by STIM1 and Orai1 in vitro and in vivo.