Hydrogen Water Protects Lungs from Radiation Damage in Study
- Authors
- Zhen Yin, Wenjing Xu, Junjun Ling, Lihai Ma, Hao Zhang, Pei Wang
- Journal
- Journal of Radiation Research
- Year
- 2024
- DOI
- 10.1093/jrr/rrae017
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Radiation Pneumonitis
- Body System
- Respiratory
TL;DR
A hydrogen-rich solution improved lung health in rats with radiation-induced lung inflammation by reducing harmful inflammation and cell damage.
Key Finding
Hydrogen-rich saline reduced lung damage and inflammation in rats with radiation-induced pneumonitis by activating cellular repair pathways and shifting immune cell behavior away from pro-inflammatory responses.
Summary
Researchers gave rats with radiation-induced lung injury (a condition that can develop after cancer treatment) a hydrogen-rich saline solution. The treatment reduced lung damage, decreased harmful inflammation, and improved cellular repair processes by reducing oxidative stress (cellular damage from unstable molecules) and changing how immune cells responded to the injury.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen-rich solutions may help protect lung tissue from radiation damage. However, these results are from rats only and have not been tested in humans, so it is too early to draw conclusions about effectiveness or safety in cancer patients receiving radiotherapy.
Abstract
This study was aimed to investigate the effect of hydrogen-rich solution (HRS) on acute radiation pneumonitis (ARP) in rats. The ARP model was induced by X-ray irradiation. Histopathological changes were assessed using HE and Masson stains. Inflammatory cytokines were detected by ELISA. Immunohistochemistry and flow cytometry were performed to quantify macrophage (CD68) levels and the M2/M1 ratio. Western blot analysis, RT-qPCR, ELISA and flow cytometry were used to evaluate mitochondrial oxidative stress injury indicators. Immunofluorescence double staining was performed to colocalize CD68/LC3B and p-AMPK-α/CD68. The relative expression of proteins associated with autophagy activation and the adenosine 5'-monophosphate-activated protein kinase/mammalian target of rapamycin/Unc-51-like kinase 1 (AMPK/mTOR/ULK1) signaling pathway were detected by western blotting. ARP decreased body weight, increased the lung coefficient, collagen deposition and macrophage infiltration and promoted M1 polarization in rats. After HRS treatment, pathological damage was alleviated, and M1 polarization was inhibited. Furthermore, HRS treatment reversed the ARP-induced high levels of mitochondrial oxidative stress injury and autophagy inhibition. Importantly, the phosphorylation of AMPK-α was inhibited, the phosphorylation of mTOR and ULK1 was activated in ARP rats and this effect was reversed by HRS treatment. HRS inhibited M1 polarization and alleviated oxidative stress to activate autophagy in ARP rats by regulating the AMPK/mTOR/ULK1 signaling pathway.