Hydrogen Gas Protects Kidneys from Muscle Damage in Rats
- Authors
- Jun-Li Xue, Bo-Yan Liu, Min Zhao, Meng-Yu Zhang, Ming-Yue Wang, Qian-Qian Gu, Xiao-Yi Zhang, Shu-Cun Qin
- Journal
- Medical Gas Research
- Year
- 2023
- DOI
- 10.4103/2045-9912.345169
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Kidney Injury
- Body System
- Renal
TL;DR
Breathing in hydrogen gas can help protect the kidneys from damage caused by a muscle injury condition called rhabdomyolysis.
Key Finding
Inhaling hydrogen gas at both 4% and 67% concentrations reduced oxidative stress, inflammation, and cell death in rat kidneys damaged by glycerol injection, with higher concentrations producing better tissue-level improvements.
Summary
Researchers tested whether breathing hydrogen gas could protect rat kidneys from damage caused by glycerol injection, which mimics a condition called rhabdomyolysis (muscle breakdown that injures the kidneys). They found that inhaling hydrogen gas at two different concentrations (4% and 67%) reduced harmful chemical reactions, inflammation, and cell death in the kidneys, with the higher concentration showing better improvement in tissue damage.
Practical Takeaway
This rat study suggests hydrogen gas inhalation may help protect kidneys from rhabdomyolysis-related injury through multiple protective mechanisms. However, this is early-stage animal research with no human trials yet, so it's unclear whether these results would apply to people or what the optimal hydrogen dose might be.
Abstract
Acute kidney injury (AKI) is the major complication of rhabdomyolysis (RM) clinically, which is usually mimicked by glycerol injection in basic research. Oxidative stress, inflammatory response and apoptosis are recognized to play important roles in development of this disease. Recently, numerous studies have reported the therapeutic effects of molecular hydrogen (H2) on oxidative stress and inflammation-related diseases. Here, the effects of H2 against glycerol-induced AKI and the underlying mechanisms were explored in rats. Low (4%) and high (67%) concentrations of H2 were prepared using a self-made device to investigate the dose-response. After 72 hours of glycerol injection (8 mL/kg), we found that glycerol triggered oxidative stress, inflammatory reactions, and apoptotic events. These caused subsequent renal damage, evidenced by a significant reduction of antioxidases and up-regulation of the relevant damaged biomarkers. H2 inhalation reversed the above alterations and exerted renoprotective effects. Interestingly, for RM/AKI-related factors, no consistent dose-response benefits of H2 were observed. However, higher concentration of H2 inhalation improved histological and morphological changes better. This study suggests that H2 is a potential alternative therapy to prevent or minimize RM induced AKI possibly via its antioxidant, anti-inflammatory, anti-apoptotic and anti-necroptotic properties.