High concentration of hydrogen ameliorates lipopolysaccharide-induced acute lung injury in a sirt1-dependent manner.
Junfeng Du, Jingwen Li, Rongqin Li, Xixin Yan · Respiratory physiology & neurobiology · 2022
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Independent study record
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H2HUBB TAKEAWAY
In mice, showed that 66.7 % hydrogen alleviated lung pathological changes and pulmonary edema caused by LPS, and reduced the degree of ALI by inhibiting pro-inflammatory cytokine release and oxidative stress response, thereby decreasing the expression of molecules related to intercellular adhesion. These results are preclinical and suggest molecular hydrogen's therapeutic potential in the condition studied. Further human research is needed to establish clinical effectiveness.
What the Researchers Studied
The study examined mice.
How Molecular Hydrogen Was Used
The aim of this study was to investigate the efficacy and underlying mechanism of high concentration of hydrogen on lipopolysaccharide (LPS)-induced acute lung injury (ALI). The pulmonary microvascular permeability and 66.7 % hydrogen on the expression of sirt1 and its downstream signaling molecules were tested.
What the Researchers Found
Showed that 66.7 % hydrogen alleviated lung pathological changes and pulmonary edema caused by LPS, and reduced the degree of ALI by inhibiting pro-inflammatory cytokine release and oxidative stress response, thereby decreasing the expression of molecules related to intercellular adhesion. sirt1 contributed to the repair of LPS-induced ALI by hydrogen through the regulation of NF-κB and catalase expression.
H₂ Mechanisms / Biological Findings
Showed that 66.7 % hydrogen alleviated lung pathological changes and pulmonary edema caused by LPS, and reduced the degree of ALI by inhibiting pro-inflammatory cytokine release and oxidative stress response, thereby decreasing the expression of molecules related to intercellular adhesion. sirt1 contributed to the repair of LPS-induced ALI by hydrogen through the regulation of NF-κB and catalase expression., 66.7 % hydrogen protected against LPS-induced ALI by suppressing inflammatory response and oxidative stress mediated by NF-κB and catalase in a sirt1-dependent manner. The aim of this study was to investigate the efficacy and underlying mechanism of high concentration of hydrogen on lipopolysaccharide (LPS)-induced acute lung injury (ALI). The pulmonary microvascular permeability and 66.7 % hydrogen on the expression of sirt1 and its downstream signaling molecules were tested.
Authors’ Conclusion
The authors concluded that , 66.7 % hydrogen protected against LPS-induced ALI by suppressing inflammatory response and oxidative stress mediated by NF-κB and catalase in a sirt1-dependent manner.