Silicon Agent Protects Kidneys by Generating Hydrogen in Rats
- Authors
- Ryoichi Imamura, Masataka Kawamura, Ayumu Taniguchi, Yuki Kobayashi, Shigeaki Nakazawa, Taigo Kato, Toyofumi Abe, Motohide Uemura, Hikaru Kobayashi, Norio Nonomura
- Journal
- Biochemical and Biophysical Research Communications
- Year
- 2020
- DOI
- 10.1016/j.bbrc.2020.10.067
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Chronic Kidney Disease
- Body System
- Renal
TL;DR
A new silicon-based treatment that releases hydrogen helps protect against kidney damage by reducing oxidative stress in rats.
Key Finding
A silicon-based hydrogen-generating agent significantly reduced kidney damage markers (serum creatinine and urinary protein) and suppressed oxidative stress in rats with advanced kidney failure.
Summary
Researchers tested a silicon-based material that generates hydrogen gas when it contacts water in the stomach. They gave this material to rats with severely reduced kidney function to see if hydrogen could help slow kidney damage. Compared to control rats, the treated rats showed lower levels of kidney damage markers, reduced signs of cellular stress, and less inflammation and cell death in kidney tissue.
Practical Takeaway
This early-stage rat study suggests hydrogen generation may help protect kidneys from oxidative stress damage, but much more research is needed before any conclusions can apply to humans. Animal studies often don't translate directly to human outcomes, so this remains preliminary evidence for a potential therapeutic approach.
Abstract
Chronic renal failure is exacerbated by oxidative stress, and this condition is difficult to treat in advanced stages. Because of the lack of effective treatments, the disease is a global public health concern. We developed a Si-based agent that continuously generates hydrogen for more than 24 h by reacting with water under conditions similar to those in the gastrointestinal tract. Given the efficacy of hydrogen in the treatment of conditions associated with oxidative stress, we examined whether the Si-based agent had beneficial effects on the development of renal failure. The Si-based agent was orally administered to rats that were developing renal failure. Rats underwent 5/6 nephrectomy to establish a remnant kidney model. Specifically, on day -7, rats underwent right 2/3 nephrectomy, followed by light nephrectomy on day 0. Starting on day -3, the rats were administered a control or Si-based agent-containing diet for 8 weeks. Compared with the findings in control rats, the Si-based agent greatly suppressed the increases of both serum creatinine and urinary protein levels. All analyzed parameters of oxidative stress were significantly suppressed in the Si-based agent groups. Histopathological examination illustrated that glomerular hypertrophy was suppressed by the treatment. Quantitative real-time reverse transcription-polymerase chain reaction revealed that sirtuin 1 and heme oxygenase-1 expression was increased in the Si-based agent groups, suggesting improved antioxidant activity and reduced hypoxia. In addition, caspase-3 and interleukin-6 expression was suppressed in the Si-based agent groups, indicating the alleviation of apoptosis and inflammation. In conclusion, oral administration of a Si-based agent resulted in renoprotective effects, presumably by suppressing oxidative stress via hydrogen generation.