Hydrogen Therapy Protects Lungs from Severe Burn Injury in Rats
- Authors
- Ning Luo, Hua Lin, Linlin Zhang, Yi Jiang, Yue Zhao, Qingqing Han, Xin Wang, Yonghao Yu, Chao Qin
- Journal
- Journal of Personalized Medicine
- Year
- 2023
- DOI
- 10.3390/jpm13030377
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Lung Injury
- Body System
- Respiratory
TL;DR
Hydrogen treatment may help reduce lung damage and inflammation caused by severe burns by preventing the self-destruction of immune cells in the lungs.
Key Finding
Hydrogen gas treatment reduced lung inflammation and decreased pyroptosis (inflammatory cell death) in alveolar macrophages of severely burned rats by suppressing a specific inflammatory pathway called NLRP3.
Summary
This study examined whether hydrogen gas could protect rat lungs from injury caused by severe burns. Researchers found that severe burns triggered a harmful process in lung immune cells called pyroptosis (a type of cell death involving inflammation). When rats were treated with hydrogen gas, the treatment reduced lung inflammation, decreased markers of cell damage, and reduced the number of damaged immune cells compared to untreated burned rats.
Practical Takeaway
This is an early-stage animal study showing hydrogen gas may help protect lungs from burn-related injury by reducing harmful inflammation. However, this research was conducted only in rats, and the study duration and sample size were not reported. Much more research, including human trials, would be needed before any conclusions could be drawn about hydrogen's usefulness for burn patients.
Abstract
Background: Hydrogen has anti-inflammatory and antioxidant effects and is beneficial to multiple organs. However, its effect on alveolar macrophage (AM) pyroptosis induced by burns is still unclear. The purpose of this research was to study the possible positive effects of hydrogen on burn-induced lung injury and the effects of hydrogen on AM pyroptosis during acute lung injury (ALI) induced by burns. Methods: In this study, histological changes in rat lungs in vivo were evaluated by micro-CT, and histological changes in isolated lungs were evaluated by hematoxylin and eosin (HE) staining. The expressions of leucine rich repeat (LRR) and pyrin domain (PYD) containing protein 3 (NLRP3), caspase-1 and Gasdermin-D (GSDMD) were analyzed by Western blotting. The expression of GSDMD was measured by immunofluorescence to evaluate the levels of lung inflammation and pyroptosis. The level of inflammation was assessed by enzyme-linked immunosorbent assay (ELISA). Pyroptosis was observed by transmission electron microscopy. Results: We observed that severe burn resulted in increased IL-1β and IL-18, overexpression of NLRP3 and caspase-1 proteins, and pyroptosis in rat lung tissues, as demonstrated by GSDMD overexpression and electron microscopy of AMs. We also observed that hydrogen treatment partially reversed the increase in lung tissue density and reduced pulmonary inflammation. Moreover, hydrogen reduced the HE pathological injury score in the lung tissues of severely burned rats. Hydrogen treatment significantly reduced the contents of IL-1β and IL-18 in the lung tissues and decreased the expression of NLRP3, caspase-1 and GSDMD proteins compared with the burn group. Transmission electron microscopy results also showed that the number of AM membrane pores was significantly reduced in the hydrogen treatment group. Conclusions: The results of this study suggest that hydrogen may protect against ALI induced by burn injury by inhibiting pyroptosis of macrophages via NLRP3.