Hydrogen-Rich Saline Inhibits Lipopolysaccharide-Induced Acute Lung Injury and Endothelial Dysfunction by Regulating Autophagy through mTOR/TFEB Signaling Pathway.
Zhiling Fu, Ze Zhang, Xiuying Wu, Jin Zhang · BioMed research international · 2020
Research-use notice
Independent study record
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H2HUBB TAKEAWAY
The results confirmed the protection of HRS in LPS-induced ALI by regulating apoptosis through inhibiting the mTOR/TFEB signaling pathway. The authors concluded that the results confirmed the protection of HRS in LPS-induced ALI by regulating apoptosis through inhibiting the mTOR/TFEB signaling pathway. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.
What the Researchers Tested
Apoptosis rate was determined by flow cytometry.
Laboratory Model
In vitro, HPMEC models of ALI were treated with LPS.
What Molecular Hydrogen Changed
The results confirmed the protection of HRS in LPS-induced ALI by regulating apoptosis through inhibiting the mTOR/TFEB signaling pathway.
Proposed Mechanism
Hydrogen-rich saline (HRS) has strong anti-inflammatory, antioxidative stress, and antiapoptotic properties.
Authors’ Conclusion
These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.