Hydrogen Water Protects Kidneys from Drug-Induced Damage in Rats
- Authors
- Yi Lu, Chun‐Fang Li, Na‐Na Ping, Yu‐Yao Sun, Zheng Wang, Gong‐Xiao Zhao, Shi‐Hui Yuan, Abdoulaye Issotina Zibrila, Lynn Soong, Jin‐Jun Liu
- Journal
- Journal of Biochemical and Molecular Toxicology
- Year
- 2020
- DOI
- 10.1002/jbt.22467
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Cyclosporine-Induced Nephrotoxicity
- Body System
- Renal
TL;DR
Drinking hydrogen-rich water (HRW) helps protect rat kidneys from damage caused by the transplant drug cyclosporine A by reducing harmful oxidative stress.
Key Finding
Hydrogen-rich water reduced kidney damage from cyclosporine A in rats by activating a cellular defense pathway (Keap1/Nrf2) that increases antioxidant enzyme activity and lowers harmful oxidative stress markers.
Summary
This study tested whether hydrogen-rich water could protect rat kidneys from damage caused by cyclosporine A, a drug used to prevent organ rejection after transplants. Researchers found that hydrogen-rich water reduced harmful molecules called free radicals in the kidneys, boosted the body's natural antioxidant defenses, and prevented kidney damage like scarring and cell death that normally occurs with long-term cyclosporine A use.
Practical Takeaway
This animal study suggests hydrogen-rich water may help protect kidneys from cyclosporine A damage, which is relevant for transplant recipients. However, this was only tested in rats, not humans, so it's unclear whether the same protective effects would occur in people. More human research would be needed before drawing any clinical conclusions.
Abstract
Oxidative stress induced by long-term cyclosporine A (CsA) administration is a major cause of chronic nephrotoxicity, which is characterized by tubular atrophy, tubular cell apoptosis, and interstitial fibrosis in the progression of organ transplantation. Although hydrogen-rich water (HRW) has been used to prevent various oxidative stress-related diseases, its underlying mechanisms remain unclear. This study investigated the effects of HRW on CsA-induced nephrotoxicity and its potential mechanisms. After administration of CsA (25 mg/kg/day), rats were treated with or without HRW (12 mL/kg) for 4 weeks. Renal function and vascular activity were investigated. Histological changes in kidney tissues were analyzed using Masson's trichrome and terminal deoxynucleotidyl transferase dUTP nick-end labeling stains. Oxidative stress markers and the activation of the Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway were also measured. We found that CsA increased the levels of reactive oxygen species (ROS) and malonaldehyde (MDA), but it reduced glutathione (GSH) and superoxide dismutase (SOD) levels. Such alterations induced vascular dysfunction, tubular atrophy, interstitial fibrosis, and tubular apoptosis. This was evident secondary to an increase in urinary protein, serum creatinine, and blood urea nitrogen, ultimately leading to renal dysfunction. Conversely, HRW decreased levels of ROS and MDA while increasing the activity of GSH and SOD. This was accompanied by an improvement in vascular and renal function. Moreover, HRW significantly decreased the level of Keap1 and increased the expression of Nrf2, NADPH dehydrogenase quinone 1, and heme oxygenase 1. In conclusion, HRW restored the balance of redox status, suppressed oxidative stress damage, and improved kidney function induced by CsA via activation of the Keap1/Nrf2 signaling pathway.