Hydrogen Inhalation Protects Kidneys from Sepsis Damage in Mice
- Authors
- Weifeng Yao, Anshun Guo, Xue Han, Shan Wu, Chaojin Chen, Chenfang Luo, Haobo Li, Shangrong Li, Ziqing Hei
- Journal
- Aging
- Year
- 2019
- DOI
- 10.18632/aging.102542
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis
- Body System
- Renal
TL;DR
Breathing in a mist containing hydrogen gas can protect the kidneys and improve survival in mice with a severe infection that leads to kidney damage.
Key Finding
Aerosol inhalation of hydrogen-rich solution protected kidney function and improved survival in septic mice by shifting immune cells from pro-inflammatory to anti-inflammatory types and reducing kidney damage.
Summary
Researchers tested whether breathing in hydrogen-rich salt water could protect kidneys in mice with sepsis (a severe infection). Septic mice developed kidney injury with high levels of inflammatory chemicals and damage to kidney cells. When given hydrogen-rich solution through inhalation, the mice showed improved kidney function, reduced inflammation, and better survival rates. The protective effect appeared to work by changing immune cells called macrophages from a pro-inflammatory type to an anti-inflammatory type.
Practical Takeaway
This early-stage mouse study suggests hydrogen-rich solution inhalation may have potential for protecting kidneys during severe infections, but results from animal studies do not directly translate to humans. Much more research, including human trials, would be needed before this approach could be considered for clinical use in sepsis patients.
Abstract
Sepsis-related acute kidney injury (AKI) is known to be caused by inflammation. We explored the renal protective effects of aerosol inhalation of a hydrogen-rich solution (HRS; hydrogen gas dissolved to saturation in saline) in a mouse model of septic AKI. Septic AKI was induced through 18 hours of cecal ligation and puncture. AKI occurred during the early stage of sepsis, as evidenced by increased blood urea nitrogen and serum creatinine levels, pathological changes, renal fibrosis and renal tubular epithelial cell apoptosis, accompanied by macrophage infiltration and M1 macrophage-associated pro-inflammatory cytokine (Il-6 and Tnf-α) generation in renal tissues. Aerosol inhalation of the HRS increased anti-inflammatory cytokine (Il-4 and Il-13) mRNA levels in renal tissues and promoted macrophage polarization to the M2 type, which generated additional anti-inflammatory cytokines (Il-10 and Tgf-β). Ultimately, aerosol inhalation of HRS protected the kidneys and increased survival among septic mice. HRS was confirmed to promote M2 macrophage polarization in lipopolysaccharide-stimulated RAW 264.7 cells. The TGF-β1 receptor inhibitor SB-431542 partly reversed the effects of HRS on renal function, fibrosis, tubular epithelial cell apoptosis and senescence in mice. Thus, HRS aerosol inhalation appears highly useful for renal protection and inflammation reduction in septic AKI.