Hydrogen Water Protects Kidneys from Damage and Scarring in Mice
- Authors
- Zhaoyu Xing, Wanma Pan, Jing Zhang, Xianlin Xu, Xuemei Zhang, Xiaozhou He, Min Fan
- Journal
- Biological & Pharmaceutical Bulletin
- Year
- 2017
- DOI
- 10.1248/bpb.b16-00832
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Chronic Kidney Disease
- Body System
- Urinary
TL;DR
Drinking hydrogen-rich water may help prevent kidney damage and scarring by blocking harmful cell changes.
Key Finding
Hydrogen-rich water reduced kidney fibrosis (scarring) and prevented kidney cells from undergoing a damaging transformation in both mouse and cell models, an effect that depended on activation of a protein called Sirt1.
Summary
Researchers tested whether hydrogen-rich water could prevent kidney damage and scarring in mice with blocked ureters (tubes that carry urine) and in human kidney cells treated with a protein that triggers scarring. Hydrogen-rich water reduced kidney scarring, preserved kidney function, and prevented kidney cells from transforming into scar-forming cells. The protective effect appeared to work through a protein called Sirt1.
Practical Takeaway
This is an early-stage animal and cell study suggesting hydrogen water may help protect against kidney scarring, but human research is needed before any health claims can be made. The study does not tell us whether these effects would occur in people or at what doses.
Abstract
The current research was designed to study the role of hydrogen in renal fibrosis and the renal epithelial to mesenchymal transition (EMT) induced by transforming growth factor-β1 (TGF-β1). Hydrogen rich water (HW) was used to treat animal and cell models. Unilateral ureteral obstruction (UUO) was performed on Balb/c mice to create a model of renal fibrosis. Human kidney proximal tubular epithelial cells (HK-2 cells) were treated with TGF-β1 for 36 h to induce EMT. Serum creatinine (Scr) and blood urea nitrogen (BUN) were measured to test renal function, in addition, kidney histology and immunohistochemical staining of alpha-smooth muscle actin (α-SMA) positive cells was performed to examine the morphological changes. The treatment with UUO induced a robust fibrosis of renal interstitium, shrink of glomerulus and partial fracture of basement membrane. Renal function was also impaired in the experimental group with UUO, with an increase of Scr and BUN in serum. After that, Western-blot was performed to examine the expression of α-SMA, fibronectin, E-cadherin, Smad2 and Sirtuin-1 (Sirt1). The treatment with HW attenuated the development of fibrosis and deterioration of renal function in UUO model. In HK-2 cells, the pretreatment of HW abolished EMT induced by TGF-β1. The down-regulation the expression of Sirt1 induced by TGF-β1 which was dampened by the treatment with HW. Sirtinol, a Sirt1 inhibitor, reversed the effect of HW on EMT induced by TGF-β1. HW can inhibit the development of fibrosis in kidney and prevents HK-2 cells from undergoing EMT which is mediated through Sirt1, a downstream molecule of TGF-β1.